الملخص
Objective:To explore the expression relationship and significance of long chain non-coding RNA nuclear-enriched abundant transcript 1(LncRNA NEAT1)and miR-27a-3p in serum and cerebro-spinal fluid of patients with Alzheimer disease(AD).Methods:Sixty-six AD patients received by the department of neurology of our hospital from October 2019 to September 2021 were gathered,according to the clinical dementia rating scale score,they were grouped into mild group(≤ 1 point,n=41)and moderate-to-severe group(＞1 point,n=25).Another 66 cases of serum and cerebrospinal fluid sam-ples from outpatient physical examination personnel were regarded as the control group.The general infor-mation on all subjects was recorded and cognition was assessed;real-time quantitative PCR was performed to measure the expression levels of miR-27a-3p and NEAT1 in serum and cerebrospinal fluid;enzyme-linked immunosorbent assay was performed to measure the protein levels of β-amyloid precursor protein cleaving enzyme 1(BACE1),β-amyloid(Aβ)40 and Aβ42 in cerebrospinal fluid;Spearman's method was performed to analyze the correlation of serum miR-27a-3p and NEAT1 levels with mini-mental state examination(MMSE)and montreal cognitive assessment(MoCA)scores;Pearson method was per-formed to analyze the correlation between serum miR-27a-3p and NEAT1 levels and Aβ deposition standard uptake value ratio(SUVR)and cerebrospinal fluid miR-27a-3p,NEAT1,BACE1,Aβ42 and Aβ40 levels.Results:The MMSE score[21(17,25),9(7,11)vs.27(21,34)],MoCA score[17(12,21),10(7,13)vs.27(21,31)],serum miR-27a-3p level(0.55±0.13,0.46±0.06 vs.0.97± 0.22),cerebrospinal fluid miR-27a-3p(0.48±0.10,0.35±0.10 vs.1.03±0.31),Aβ42 levels[(303.55±36.77)ng/L,(231.45±34.14)ng/L vs.(499.99±53.63)ng/L]and Aβ42/Aβ40 ra-tio(0.030±0.008,0.022±0.007 vs.0.048±0.010)of AD patients in mild group and moderate-to-severe group were all lower than those in the control group,and the moderate-to-severe group were lower than the mild group(all P＜0.05);the serum NEAT1 level(2.31±0.64,3.13±0.76 vs.1.05± 0.20),SUVR(1.50±0.29,1.76±0.52 vs.0.74±0.15),and cerebrospinal fluid NEAT1(3.51± 1.24,4.30±1.65 vs.1.01±0.23)and B ACE 1 levels[(55.78±5.98)μg/L,(72.32±16.08)μg/L vs.(21.39±3.73)μg/L]were higher than those in the control group,and the moderate-to-se-vere group were higher than the mild group(all P＜0.05).Serum NEAT1 level in AD patients was posi-tively correlated with SUVR,cerebrospinal fluid NEAT1 and BACE1(r=0.350,0.606,0.341,P＜0.05),and negatively correlated with MMSE score and MoCA score(r=-0.473,-0.482,all P＜0.05);serum miR-27a-3p level was positively correlated with cerebrospinal fluid miR-27a-3p level,MMSE score and MoCA score(r=0.695,0.424,0.412,all P＜0.05),and negatively correlated with SUVR and cerebrospinal fluid BACE1 level(r=-0.521,-0.447,all P＜0.05).Conclusion:The expression trends of NEAT1 and miR-27a-3p in the serum and cerebrospinal fluid of AD patients are con-sistent,the level of NEAT1 is increased,and the level of miR-27a-3p is decreased.The levels of the two are negatively correlated,which is related to the degree of Aβ deposition in the brain of AD patients and is involved in the progression of AD.
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Objective To investigate the relationship between serum levels of long non-coding RNA(ln-cRNA)nuclear-enriched abundant transcript 1(NEAT1)and microRNA miR-23c in patients with diabetic ne-phropathy(DN).Methods A total of 136 DN patients admitted to the hospital from May 2019 to May 2020 were enrolled in the study as the DN group.Fifty-eight healthy people who underwent physical examination in the hospital during the same period were enrolled as the control group.Real-time fluorescence quantitative PCR(qPCR)was used to detect serum lncRNA NEAT1,miR-23c,kidney injury molecule-1(KIM-1),neutro-phil gelatinase-associated lipocalin(NGAL),tumor necrosis factor-α(TNF-α)mRNA and interleukin-6(IL-6)mRNA in the two groups.Pearson/Spearman correlation was used to analyze the correlation of serum ln-cRNA NEAT1 and miR-23c with KIM-1,NGAL,TNF-α,IL-6 mRNA levels and eGFR in DN patients.DN pa-tients were divided into different CKD stages,and the levels of serum lncRNA NEAT1,miR-23c,KIM-1,NGAL,TNF-α,and IL-6 mRNA in patients in different CKD stages were compared.Multivariate ordered Lo-gistic regression was used to analyze whether serum levels of lncRNA NEAT1 and miR-23c were influencing factors for the progression of DN.Results Compared with the control group,the serum levels of lncRNA NEAT1,KIM-1,NGAL,TNF-α and IL-6 mRNA in the DN group were increased,while miR-23c and esti-mated glomerular filtration rate(eGFR)were decreased,and the differences were all statistically significant(P＜0.05).The serum levels of lncRNA NEAT1,KIM-1,NGAL,TNF-α and IL-6 mRNA in DN patients in G1-G5 stages were increased in order,and the level of miR-23c was decreased in order(P＜0.05).Serum ln-cRNA NEAT1 in DN patients was positively correlated with KIM-1,NGAL,TNF-α and IL-6 mRNA levels(P＜0.05),and negatively correlated with miR-23c and eGFR(P＜0.05).The level of serum miR-23c was negatively correlated with the mRNA levels of KIM-1,NGAL,TNF-α and IL-6(P＜0.05),and positively cor-related with eGFR(P＜0.05).lncRNA NEAT1(OR=2.177,95％CI:2.113-2.441)was an independent risk factor for DN progression,while miR-23c(OR=0.595,95％CI:0.543-0.726)was an independent pro-tective factor(P＜0.05).Conclusion Elevated serum lncRNA NEAT1 levels and reduced miR-23c levels in DN patients are closely associated with the progression of DN disease.
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Objective:To evaluate the effect of long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) on the radiosensitivity in breast cancer cells by regulating the miR-149-5p/ glutamic pyruvic transaminase 2 (GPT2) axis.Methods:Real-time reverse transcription PCR (RT-qPCR) was used to detect NEAT1, miR-149-5p and glutamic pyruvic transaminase 2 (GPT2) mRNA levels in human breast cells MCF-10A, and human breast cancer cells MCF-7, MDA-MB-231 and MDA-MB-468, respectively. MCF-7 cells were divided into 0, 2, 4, 6 and 8 Gy irradiation groups. MCF-7 cells were divided into NEAT1 knockdown (si-NEAT1) group and control (si-NC) group, NEAT1 knockdown +miR-149-5p knockdown (si-NEAT1+anti-miR-149-5p) group and control (si-NEAT1+anti-miR-NC) group, NEAT1 knockdown + GPT2 overexpression (si-NEAT1+GPT2) group and control (si-NEAT1+NC) group. On the basis of the above grouping, irradiate each group of cells with 4 Gy radiation for 2 h, denoted as IR+si-NEAT1, IR+si-NC, IR+si-NEAT1+anti-miR-149-5p, IR+si-NEAT1+anti-miR-NC, IR+si-NEAT1+GPT2, IR+si-NEAT1+NC groups. Subsequently, MCF-7 cells were irradiated at a dose of 4 Gy and divided into the IR+si-NEAT1, IR+si-NC, IR+si-NEAT1+anti-miR-149-5p, IR+si-NEAT1+anti-miR-NC, IR+si-NEAT1+GPT2 and IR+si-NEAT1+NC groups. RT-qPCR was used to detect NEAT1, miR-149-5p, GPT2 mRNA levels in cells. Colony formation assay was used to detect cell radiosensitivity. CCK-8 assay was adopted to detect cell proliferation ability. The binding sites of NEAT1 and miR-149-5p were predicted by StarBase database. The binding sites of miR-149-5p and GPT2 were predicted by Targetscan database, and validated by dual luciferase assay. Single factor ANOVA was used for inter-group comparisons. LSD- t test was used for pairwise comparison. Results:Compared with MCF-10A cells, NEAT1 and GPT2 mRNA levels in cell lines were up-regulated, whereas miR-149-5p level was down-regulated (all P<0.05). Compared with the 0 Gy dose group, NEAT1 and GPT2 mRNA levels were down-regulated, while miR-149-5p levels were up-regulated in the 2, 4, 6, and 8 Gy dose groups (all P<0.05). Knockdown of NEAT1 expression or radiation alone could enhance cell radiosensitivity, and reduce cell proliferation ability (all P<0.05). Simultaneous radiation treatment with knockdown of NEAT1 expression could strengthen the above effects upon cells (all P<0.05). Knockdown of miR-149-5p expression or overexpression of GPT2 could partially reverse the aforementioned effects of knockdown of NEAT1 expression (all P<0.05). Conclusion:Knockdown of NEAT1 expression enhances breast cancer cell radiosensitivity, and reduces cell proliferation ability by regulating the miR-149-5p/GPT2 signal axis.
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ObjectiveAlthough expression of the TEAD1 protein in preadipocytes has been established, its function remains unclear. In this study, we sought to detect transcripts of TEAD1 in chicken and to examine the effects of this protein on the proliferation, migration, apoptosis, and differentiation of immortalized chicken preadipocyte cell lines (ICP1). MethodsThe full-length sequence of the TEAD1 gene was cloned and the two transcripts were subjected to bioinformatics analysis. The subcellsular localization of TEAD1 transcripts was determined based on indirect immunofluorescence. The effects of TEAD1 transcripts overexpression on the proliferation of ICP1 cells were examined by RT-qPCR, CCK-8, and EdU assays; the effects of TEAD1 transcripts on ICP1 cells migration were examined based on the scratch test; and the effects of TEAD1 transcripts overexpression on ICP1 cells apoptosis were analyzed using apoptosis-Hoechst staining and RT-qPCR. The expression of TEAD1 transcripts in different tissues, cells lines, and ICP1 at different periods of differentiation was analyzed by RT-qPCR. The effects of TEAD1 transcripts overexpression on lipid droplet accumulation and adipogenic-related gene expression in ICP1 cells were analyzed based on Oil Red O and BODIPY staining, RT-qPCR, Western blot, and dual-luciferase reporter gene assays. Finally, the content of triglyceride (TG) was measured in TEAD1 overexpressed ICP1 cells. ResultsThe full-length TEAD1 was cloned and two TEAD1 transcripts were identified. The TEAD1-V1 protein was found to be localized primarily in the cell nucleus, whereas the TEAD1-V2 protein is localized in the cell cytoplasm and nucleus. The overexpression of both TEAD1-V1 and TEAD1-V2 significantly inhibited the proliferation of ICP1 cells. Whereas the overexpression of TEAD1-V1 promoted ICP1 cell migration, the overexpression of TEAD1-V2 had no significant effects on ICP1 migration; the overexpression of both TEAD1-V1 and TEAD1-V2 significantly promoted the apoptosis of ICP1 cells. We found that the different transcripts of TEAD1 have similar expression pattern in different tissues and cells lines. During induced preadipocyte differentiation, the expression of these genes initially declined, although subsequently increased. Overexpression of TEAD1-V1 promoted a significant reduction in lipid droplet formation and inhibited C/EBPα expression during the differentiation of ICP1 cells (P<0.05). However, the overexpression of TEAD1-V2 had no significant effect on lipid droplet accumulation or the expression of adipogenic-related proteins (P>0.05). Overexpression of TEAD1-V1 significantly decreased triglyceride content in ICP1 cells (P<0.05), while overexpression of TEAD1-V2 had no effect on triglyceride content in ICP1 cells (P>0.05). ConclusionIn this study, for the first time, identified two TEAD1 transcripts. Overexpressed transcripts TEAD1-V1 and TEAD1-V2 both inhibited the proliferation of chicken preadipocytes and promoted apoptosis of chicken preadipocytes. TEAD1-V1 inhibited the differentiation of preadipocytes and promoted the migration of preadipocytes, while TEAD1-V2 had no effect on the differentiation and migration of preadipocytes.
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AIM: To detect the expression levels of long non-coding RNA(lncRNA)X-inactive specific transcript(XIST)and silencing information regulatory factor 2 associated enzyme 1(SIRT1)in serum of patients with type 2 diabetes mellitus(T2DM), and to explore their correlation with diabetic retinopathy(DR)and their diagnostic value. METHODS: Prospective study. A total of 214 patients with T2DM admitted to our hospital from January 2022 to February 2023 were selected as the research subjects. Based on whether retinopathy occurred, they were divided into 126 cases(126 eyes)in the non-DR group and 88 cases(88 eyes)in the DR group. An additional 130 healthy individuals who underwent a physical examination during the same period were selected as the control group. The serum levels of lncRNA XIST and SIRT1 in the three groups were measured and compared. The relationship between lncRNA XIST and SIRT1 expression with DR was analyzed using Pearson's method. The receiver operating characteristic(ROC)curve was used to evaluate the predictive value of serum lncRNA XIST, SIRT1, and their combination for DR. Multivariate Logistic regression analysis was performed to investigate the factors affecting the occurrence of DR in T2DM patients.RESULTS: Compared with the control group, the levels of serum lncRNA XIST and SIRT1 in the non-DR group and DR group were successively decreased(all P<0.05). The levels of serum lncRNA XIST and SIRT1 were positively correlated in DR patients(r=0.639, P<0.05). ROC analysis showed that the area under the curve(AUC)for predicting DR by combining serum lncRNA XIST and SIRT1 was 0.940, which was higher than the AUC by serum lncRNA XIST and SIRT1 alone(0.855, 0.875). Logistic regression analysis showed that lncRNA XIST(OR=0.752)and SIRT1(OR=0.694)were influencing factors for the occurrence of DR(both P<0.01).CONCLUSION: The serum levels of lncRNA XIST and SIRT1 are both lower in DR patients, and the combination of lncRNA XIST and SIRT1 has a better assessment capacity for the occurrence of DR.
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Abstract Objective: Chronic Rhinosinusitis with Polyps (CRSwNP) is characterized by high heterogeneity and postoperative recurrence rate. This study aims to explore the clinical significance of tissue Leukocyte-Specific Transcript 1 (LST1) in predicting CRSwNP recurrence. Methods: We enrolled 62 CRSwNP patients including 30 primary CRSwNP and 32 recurrent CRSwNP patients, and 40 Healthy Controls (HC). Tissue samples were collected. Tissue LST1 expression was assessed by Reverse Transcription-Polymerase Chain Reaction (RT-PCR), Western Blotting (WB) and Immunofluorescence (IF) staining. The predictive values of LST1 expression for CRSwNP postoperative recurrence were assessed through the Receiver Operating Characteristic (ROC) curves. Results: The tissue levels of LST1 were significantly increased in the CRSwNP group than the HC group, especially in the recurrent group, and the elevated LST1 mRNA levels were positively correlated with the peripheral eosinophil percentages, tissue eosinophil counts and percentages. IF staining results showed that the LST1 protein levels were higher in CRSwNP patients, especially in the recurrent patients than in the HC group. ROC curves highlighted that tissue LST1 levels were associated with recurrent CRSwNP and exhibited a higher predictive ability for postoperative CRSwNP recurrence. Conclusion: This was the first report suggesting that LST1 expression was upregulated and associated with mucosal eosinophil infiltration and CRSwNP recurrence. Tissue LST1 could be a promising biomarker for predicting postoperative recurrence in CRwNP patients.
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【Objective】 To establish RH gene mRNA sequencing method based on nanopores sequencing and to explore the RHD and RHCE mRNA transcripts in D positive and Del individuals. 【Methods】 From March 2021 to May 2022, 5 RhD positive samples and 5 Del samples screened out by hospitals in Chengdu were sent to our laboratory for futher examination. The erythrocytes and buff coat were isolated, then DNA and RNA were extracted.All 10 samples were genotyped by PCR-SSP. After the mRNA was reversely transcribed into cDNA, the full-length mRNA of RHD and RHCE genes were simultaneously amplified by a pair of primers. Sanger sequencing and third-generation sequencing technology based on Nanopore were used to sequence the amplified products, and the types and expressions of different splices of RHD and RHCE gene mRNA transcripts were analyzed. 【Results】 The method established in this study can simultaneously amplify the full length transcripts of RHD and RHCE. Ten different RHD gene mRNA transcripts and nine RHCE gene mRNA transcripts were detected in 10 samples. RHD full-length transcript (RHD-201) can be detected in RhD Del type, but the expression amount was significantly lower than that in RhD positive samples. The expression amount of transcript RHD-207 (Del789) in Del samples was significantly higher than that in RhD positive samples. The transcript RHD-208 (Del8910+ 213) was only detected in RhD Del type individuals, and no significant difference was found between other RHD transcripts and all RHCE transcripts in the two phenotypes. 【Conclusion】 In this study, an analytical method for sequencing full-length transcript isomers of RHD and RHCE mRNA via the third generation was successfully established, and complex alternative splicing patterns were found in RHD and RHCE genes, providing a new method for the study of alternative splicing of blood group gene variants mRNA.
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Objective:To explore the distribution of the copy number of survival motor neuron gene 2 ( SMN2) and the transcript level of the full-length SMN2 ( fl-SMN2) transcript level in patients with type 1-3 spinal muscular atrophy (SMA), and to evaluate their influences on disease severity, progression, and prognosis. Methods:It was a retrospective study involving 78 therapy-naive SMA patients with SMN1 gene homozygous deletion who were diagnosed and treated in the Capital Institute of Pediatrics from January 2019 to December 2021.Cross-sectional clinical data, including age at onset, motor milestones, and complications were recorded.They were followed up for monitoring motor function degeneration and survival.The copy number of SMN2 and the transcript level of fl-SMN2 were detected.Differences between groups were compared by the Student′s t-test or One- Way ANOVA or Chi- square test.Kaplan-Meier analysis was used for survival analysis, and Kendall′ s tau- c was performed to assess the correlation of these two biomarkers with SMA phenotypes, age at onset, motor milestones, and survival. Results:Of the 78 SMA patients, there were 17 cases (21.8%) of type 1, 34 cases(43.6%) of type 2, and 27 cases(34.6%) of type 3.Seven cases(41.2%) type 1 SMA patients died, with a median survival time of 11 months, and no deaths were observed in type 2 and type 3 SMA patients.There was a significant difference in the median age at onset among SMA patients with 2, 3, and 4 copies of SMN2 (1.8, 12.0, and 24.0 months, respectively; F=4.943, P=0.01). The mean transcript level of fl-SMN2 in type 1, 2 and 3 SMA patients were 196.25±68.79, 331.21±108.79 and 455.69±122.27, respectively ( F=37.154, P<0.001). The survival rate of SMA with 2 SMN2 copies at 1, 2, and 5 years were 50.5%, 0, and 0, respectively, and their median survival age was 7 months.The survival rate of SMA with 3 and 4 SMN2 copies at 5 years were 97.4% and 100.0%, respectively.Moreover, a negative correlation was observed between the transcript level of fl-SMN2 and phenotype severity ( Kendall′ s tau- c=-0.444, P<0.001), and the transcript level of fl-SMN2 of the survival group was much higher than that of the death group (342.93±125.74 vs.212.14±92.31). More copies of SMN2 and higher transcript level of fl- SMN2 indicated more motor function acquisitions (head control, sitting and walking) ( P<0.001). In addition, there was a significant difference in the transcription level of fl-SMN2 between the undegenerated group and the degenerated group in sitting and standing ( F=5.432, P=0.023 and F=4.315, P=0.047, respectively). Conclusions:Both the copy number of SMN2 and the transcript level of fl-SMN2 are correlated with SMA severity, survival, and motor milestones, serving as valuable biomarkers for evaluating phenotypic severity of SMA.The transcript level of fl-SMN2 s may play an important role in the degeneration of sitting and standing.
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@#Objective To investigate the effect of long noncoding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) silencing on cerebral ischemia reperfusion injury (CIRI) in rats by regulating microglia polarization through interleukin (IL)-10/signal transducer and activator of transcription 3 (STAT3) signaling pathway.Methods SD rats were randomly divided into sham operation group (Sham group),CIRI group,CIRI+si-NC group,CIRI+si-NEAT1 group,each group of 24 rats.Except for the Sham group,the rats in the other groups were used to construct the CIRI model by thread occlusion method.After modeling,rats in each group were given corresponding treatments for 7 days.Neurological deficits of rats were scored; brain histopathological changes were observed; the percentage of cerebral infarction volume,the number of M1 and M2 polarization marker positive (Iba1+CD86+,Iba1+CD206+) cells in the positive cells of ionic calcic junction protein molecule 1 (Iba1+),IL-1β,tumor necrosis factor-α (TNF-α),IL-4,IL-10,lncRNA NEAT1,inducible nitric oxide synthase (iNOS),arginase-1 (Arg-1),IL-10 mRNA,IL-10,STAT3,phosphorylated STAT3 (p-STAT3) protein levels in rat brain tissue were detected.Results Compared with Sham group,the CIRI group showed severe pathological damage of brain tissue in rats,neurological deficit score,percentage of cerebral infarction volume,number of Iba1+CD86+,Iba1+CD206+ positive cells,CD86/CD206 ratio,IL-1β,TNF-α,IL-4,IL-10 levels,lncRNA NEAT1,iNOS,Arg-1,IL-10 mRNA levels,IL-10 and p-STAT3/STAT3 protein levels in brain tissue were significantly increased (P<0.05);compared with CIRI group and CIRI+si-NC group,CIRI+si-NEAT1 group had less pathological damage of brain tissue in rats,neurological deficit score,percentage of cerebral infarction volume,number of Iba1+CD86+ positive cells,CD86/CD206 ratio,IL-1β and TNF-α levels,lncRNA NEAT1,iNOS mRNA levels in brain tissue were significantly decreased (P<0.05),the number of Iba1+CD206+cells,IL-4,IL-10 levels,Arg-1,IL-10 mRNA,IL-10 and p-STAT3/STAT3 protein levels were significantly increased (P<0.05). Conclusion Silencing lncRNA NEAT1 may regulate microglial polarization by activating IL-10/STAT3 signaling pathway,thereby ameliorating brain tissue injury in CIRI rats.
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@#Objective To construct eukaryotic expression plasmids of human promyelocytic leukaemia(hPML) gene of six transcripts and analyze the subcellular location of the recombinant proteins.Methods Primers were designed according to the hPML gene sequences registered in GenBank databases.Six transcripts of hPML gene fragments(hPML Ⅰ,Ⅱ,Ⅳ,Ⅴ,Ⅵ and Ⅶ) were amplified by RT-PCR,which were linked to the eukaryotic expression vector pCAGGS respectively.The obtained eukaryotic expression plasmids of six transcripts of hPML gene were transfected into 293T cells respectively and detected for their protein expression by Western blot,while transfected into Vero cells and detected for their subcellular location by indirect immunofluorescence assay(IFA).Results The target gene fragments of the six eukaryotic expression plasmids were consistent with the hPML gene sequences registered in GenBank.All the six recombinant proteins showed specific binding with Myc antibody,among which the recombinant protein hPML Ⅰ,Ⅱ,Ⅳ,Ⅴ and Ⅵ were located in the nucleus and cytoplasm,while the recombinant protein hPML Ⅶ was mainly located in the cytoplasm,rarely in the nucleus.Conclusion The eukaryotic expression plasmids of six transcripts of hPML gene all can be expressed correctly in mammalian cells,and the expressed recombinant proteins were located in nucleus and cytoplasm simultaneously or mainly in cytoplasm.This study provides an experimental basis for subsequent study on the antiviral and other biological functions of recombinant protein hPML.
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@#Objective To investigate the effects of long non-coding RNA(LncRNA) growth arrest specific transcript 5(GAS5) negatively regulating nucleophosmin 1(NPM1) on cisplatin(DDP) resistance of gastric cancer cells.Methods The normal human gastric mucosa cell line GES-1 and human gastric cancer cell lines BG3-823,MGC-803 and AGS were selected as the research objects,of which the level of LncRNA GAS5 in each cell was measured by qRT-PCR.The drug resistance of AGS cells to DDP(AGS/DDP) was induced,and the experiment was divided into control group,empty plasmid group(BC group),GAS5 nonsense interference group(pLJM-GAS5 NC group) and GAS5 overexpression group(pLJM-GAS5 group).MTT method was used to determine the effect of DDP on the proliferation of AGS and AGS/DDP cells;and the levels of NPM1,multidrug resistance 1(MDR1),excision repair cross complementation group 1(ERCC1),multidrug resistance-associated protein 1(MRP1) and N-cadherin in AGS and AGS/DDP cells were measured by Western blot.Results Compared with the normal gastric mucosa GES-1 cells,the level of LncRNA GAS5 in BG3-823 and AGS cells decreased significantly,and among them,the level of LncRNA GAS5 in AGS cells was the lowest,so AGS cells were used for the follow-up experiments.Compared with the control group,the level of LncRNA GAS5 in AGS cells of BC group and pLJM-GAS5 NC group decreased significantly,while the levels of NPM1,MDRl,ERCC1,MRP1 and N-cadherin increased significantly;compared with BC group and pLJM-GAS5 NC group,the level of LncRNA GAS5 in AGS/DDP cells of pLJM-GAS5 group increased significantly,while the levels of NPM1,MDR1,ERCC1,MRP1 and N-cadherin decreased significantly;after treatment with DDP of the same concentration(except 0 μmol/L),compared with the control group,the inhibition rate of AGS/DDP cell proliferation in BC group and pLJM-GAS5 NC group decreased significantly;compared with BC group and pLJM-GAS5 NC group,the inhibition rate of AGS/DDP cell proliferation in pLJM-GAS5group was significantly higher.The semi inhibitory concentration(IC_(50)) of DDP on AGS/DDP cells in pLJM-GAS5 group for 48 h was(65.38±5.04) μmol/L,which was significantly lower than(120.74±4.17) μmol/L and(120.24±4.29) μmol/L in BC group and pLJM-GAS5 NC group.Conclusion Up-regulating the level of LncRNA GAS5 in AGS/DDP cells can reverse the drug resistance of AGS/DDP cells,which may be related to the down-regulation of NPM1expression
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OBJECTIVE To investigate the association between the functional GLCCI1 gene rs37973 polymorphism and inhaled corticosteroids （ICSs） response in patients with asthma-chronic obstructive pulmonary disease overlap （ACO）. METHODS Totally 173 newly diagnosed ACO patients were recruited from Shanghai Pudong New Area People’s Hospital during April 1st， 2019 to December 31st， 2020. All patients were treated with Salmeterol fluticasone inhalation powder， twice a day， for 24 weeks. The genotype of rs37973 locus was determined， and lung function indicators [forced expiratory volume in one second （FEV1）， FEV1/forced vital capacity （FVC）， the percentage of FEV1 to expected value （FEV1%pred）]， and lung function improvement （ΔFEV1 and ΔFEV1%pred） were all detected. RESULTS Totally 111 patients completed the whole 24-week follow-up and lung function detection. Among them， there were 42 cases of AA genotype， 52 cases of AG genotype， and 17 cases of GG genotype. After 12， 24 weeks of treatment， lung function indexes of patients were significantly better than baseline lung function indexes before treatment （P＜0.05）. After 24 weeks of treatment， ACO patients with AA and AG genotypes showed significantly better lung function improvement than GG genotype， and ΔFEV1%pred of AA genotype was significantly better than AG genotype （P＜ 0.05）. After 12， 24 weeks of treatment， the improvement of lung function in patients with a smoking history ≤20 pack year was significantly better than those with a smoking history ＞20 pack year， and among patients with a smoking history ≤20 pack year， only AA genotype had significantly better FEV1%pred than AG genotype （P＜0.05）. After 12 weeks of treatment， among patients with a smoking history ＞20 pack year， the improvement of lung function in AA genotype and AG genotype was significantly better than GG genotype， and the FEV1%pred in AA genotype was significantly better than AG genotype （P＜0.05）. After 24 weeks of treatment， the improvement of lung function of AA genotype and AG genotype was significantly better than GG genotype （P＜0.05）. CONCLUSIONS GG genotype of GLCCI1 gene rs37973 locus is associated with the poor treatment response to ICSs in patients with ACO， especially in patients with smoking history ＞20 pack year.
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Objective:To investigate the effects of long noncoding RNA (LncRNA) lung cancer associated transcript 1 (LUCAT1) targeting microRNA (miR)-502-5p on the proliferation, migration and invasion of human retinoblastoma (RB) cells.Methods:RB tissue samples were collected from 27 RB patients who underwent eyeball enucleation in Henan Eye Hospital from May 2019 to January 2021.Another 27 normal retinal tissue specimens were collected from 12 patients with eyeball rupture, 7 with eyeball atrophy, and 8 with eyeball penetrating injury combined with pigment film incarceration who underwent the eyeball enucleation in Henan Eye Hospital during the same period.The expressions of LncRNA LUCAT1 and miR-502-5p in RB tissues, cell lines (Y-79, WERI-Rb-1, HXo-RB44) and human retinal epithelial cells (ARPE-19) were detected by real-time quantitative PCR.Y-79 RB cell was divided into control group, small interfering RNA (si)-LncRNA LUCAT1 group, si-control (con) group, pcDNA group, pcDNA-LncRNA LUCAT1 group, miR-con group, miR-502-5p group, si-LncRNA LUCAT1+ anti-miR-con group and si-LncRNA LUCAT1+ anti-miR-502-5p group, and cells in different groups were transfected with corresponding reagents.The expressions of MMP2 and MMP9 proteins were detected by Western blot.Cell proliferation activity was assayed by cell counting kit 8.Cell proliferation capability was detected by colony formation assay.Cell migration and invasion ability were determined by Transwell assay.The targeting regulation of LncRNA LUCAT1 against miR-502-5p was confirmed by dual luciferase reporter assay and real-time quantitative PCR.The study protocol was approved by the Ethics Committee of Henan Eye Hospital (No.HNEECKY-2021[32]). Written informed consent was obtained from guardians of subjects.Results:LncRNA LUCAT1 expression level in RB tissue was 2.73±0.34, which was significantly higher than 1.00±0.15 in normal retinal tissue ( t=24.190, P<0.001). The miR-502-5p expression level in RB tissues was 0.42±0.06, which was significantly lower than 1.00±0.13 in normal retinal tissue ( t=21.049, P<0.001). LncRNA LUCAT1 expression level was significantly higher and the miR-502-5p expression level was significantly lower in human RB cell lines Y-79, WERI-Rb-1 and HXO-RB44 than those in ARPE-19 cells, with statistically significant differences (all at P<0.05). The LncRNA LUCAT1 expression, the relative expressions of MMP2 and MMP9 proteins, the absorbance ( A) value, and the number of proliferated, migrating and invading Y-79 cells in si-LncRNA LUCAT1 group were significantly reduced in comparison with control group, and the differences were statistically significant (all at P<0.05). The miR-502-5p expression level was higher, and the relative expression levels of MMP2 and MMP9, A value, as well as the number of proliferated, migrating and invading Y-79 cells were lower in miR-502-5p group than in miR-con group, showing statistically significant differences ( t=20.274, 14.884, 14.181, 12.692, 17.749, 20.889, 21.913; all at P<0.001). The miR-502-5p expression level was lower and the relative expression levels of MMP2 and MMP9, A value as well as the number of proliferated, migrating and invading Y-79 cells were higher in si-LncRNA LUCAT1+ anti-miR-502-5p group than in si-LncRNA LUCAT1+ anti-miR-con group, showing statistically significant differences ( t=14.097, 15.839, 15.757, 11.860, 16.235, 16.565, 16.487; all at P<0.001). When co-transfected with LncRNA LUCAT1-wild type, the relative luciferase activity of miR-502-5p group was lower than that of miR-con group, and the difference was statistically significant ( t=16.379, P<0.001). The LncRNA LUCAT1 expression level was higher and the miR-502-5p expression level was lower in pcDNA-LncRNA LUCAT1 group than in pcDNA group, and the differences were statistically significant (both at P<0.05). The LncRNA LUCAT1 expression level was lower and the miR-502-5p expression level was higher in si-LncRNA LUCAT1 group than in si-con group, and the differences were statistically significant (both at P<0.05). Conclusions:Inhibition of LncRNA LUCAT1 can attenuate the proliferation, migration and invasion ability of human RB cells by the targeting up-regulation of miR-502-5p.
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Objective:To investigate the expression of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1(lncRNA MALAT1) in bronchopulmonary dysplasia (BPD) of neonatal rats induced by hyperoxia and its effect on alveolar type 2 epithelial cells (AEC Ⅱ).Methods:The lung injury model of neonatal SD rats induced by hyperoxia(model group, n=50, inhaled oxygen concentration of 80%-85%) and the control group(inhaled air, n=50) were prepared.Lung tissue samples were taken and retained on days 1, 3, 7, 14 and 21, and the physiological and pathological changes of lung tissue were detected by paraffin-embedded sections and hematoxylin-eosin staining; The dynamic expression of lncRNA MALAT1 in lung tissue was detected by real-time fluorescent quantitative polymerase chain reaction; The dynamic expression of surfactant protein C(SPC) in lung tissue and AECⅡ was detected by Western blot.AECⅡ was extracted from lung tissue of normal newborn rats, and lncRNA MALAT1 was knocked down by siRNA.The cells were collected and Western blot as well as immunofluorescence were used to detect the changes of SPC. Results:The lung tissue of model group gradually became thickened with alveolar compartments, and the alveolar cavity was enlarged with the disappearance of alveolar spine and other pathological structural changes.Compared with the control group, there was no difference in the expression of lncRNA MALAT1 and SPC in the lung tissue from model group on days 1, 3( P>0.05), but the expression of lncRNA MALAT1 and SPC significantly increased on days 7, 14 and 21( P<0.05). When lncRNA MALAT1 was inhibited, SPC expression showed a decrease trend. Conclusion:Hyperoxia can lead to the stagnation of lung development in neonatal rats, and the structure and function of alveolar disorders are impaired.The expression of lncRNA MALAT1 is involved in the process of hyperoxia-induced BPD in neonatal rats.The increase of lncRNA MALAT1 may promote the proliferation of AECⅡ.
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Objective:To explore the inhibitory effect of long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) by targeting microRNA-199a-5p (miR-199a-5p) on the apoptosis of human lens epithelial cells (LECs).Methods:The anterior lens capsule tissue of 23 age-related cataract patients who underwent cataract surgery in Xinxiang First People's Hospital from December 2018 to August 2019 was collected.At the same time, anterior lens capsules from 20 healthy donor were collected.The expressions of KCNQ1OT1 and miR-199a-5p in the tissues were detected by real-time fluorescence PCR.Human LECs SRA01/04 cultured in vitro were divided into blank control group, model control group, small interfering RNA-negative control (siR-NC) group, siR-KCNQ1OT1 group, miR-NC group, miR-199a-5p group, siR-KCNQ1OT1+ anti-miR-NC group and siR-KCNQ1OT1+ anti-miR-199a-5p group.No intervention was administered to blank control group.Cells in model control group were cultured with 100 μmol/L H 2O 2 for 24 hours to establish oxidative stress injured model, and cells in the other six groups were transfected with corresponding transfection reagents for 6 hours by liposome method according to grouping, and then treated with 100 μmol/L H 2O 2 for 24 hours.The expressions of KCNQ1OT1 and miR-199a-5p in lens anterior capsule tissue and LECs cells were determined by real-time fluorescent quantitative PCR.Cell viability was detected with thiazolyl blue (MTT). Cell apoptosis was analyzed by flow cytometry.The expressions of B-cell lymphoma/leukemia-2 (bcl-2) and bcl-2 related X protein (Bax) proteins were assayed by Western blot.The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured by enzyme-linked immunosorbent assay (ELISA). The targeting relationship between KCNQ1OT1 and miR-199a-5p was verified by dual luciferase reporter experiment.The study protocol was approved by an Ethics Committee of Xinxiang First People's Hospital (No.2019-001). Written informed consent was obtained from relatives of patient. Results:The relative expression of KCNQ1OT1 in the anterior capsule of patients with age-related cataract was 2.41±0.42, which was significantly higher than 0.97±0.19 of normal people, and the relative expression of miR-199a-5p in the capsule of patients with age-related cataract was 0.36±0.12, which was lower than 1.04±0.15 of normal people, and the differences were statistically significant ( t=14.112, 16.507; both at P<0.001). Compared with blank control group, the relative expressions of KCNQ1OT1 and bax protein, cell apoptosis rate and MDA content were significantly increased, and the relative expressions of miR-199a-5p and bcl-2 protein, cell viability and SOD activity were significantly reduced in model control group, showing statistically significant differences (all at P<0.001). Compared with siR-NC group, the relative expressions of KCNQ1OT1 and bax protein, cell apoptosis rate and MDA content in cells of siR-KCNQ1OT1 group were decreased, while the relative expression of bcl-2 protein, cell survival rate and SOD activity were increased, and the differences were statistically significant (all at P<0.05). Compared with miR-NC group, the KCNQ1OT1-wild type (WT) luciferase activity in miR-199a-5p group was significantly decreased, with a statistically significant difference ( t=21.131, P<0.001). The relative expression levels of miR-199a-5p and bcl-2 proteins, cell survival rate and SOD activity were significantly increased, and the relative expression of bax protein, cell apoptosis rate and MDA content were significantly decreased in miR-199a-5p group than those in miR-NC group, and the differences were statistically significant (all at P<0.05). The relative expression levels of miR-199a-5p and bcl-2 proteins, cell survival rate and SOD activity were significantly lower, and the cell apoptosis rate, relative expression of bax protein and MDA content were significantly higher in siR-KCNQ1OT1+ anti-miR-199a-5p group than those in siR-KCNQ1OT1+ anti-miR-NC group, and the differences were statistically significant (all at P<0.05). Conclusions:The inhibition of KCNQ1OT1 can promote the cell viability of human LECs, inhibit H 2O 2-induced cell apoptosis and oxidative stress, and the mechanism may be related to the up-regulation of miR-199a-5p.
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Objective:To investigate the correlations between expression of long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), nuclear-enriched abundant transcript 1 (NEAT1) and their functions on exosome secretion, proliferation and invasion in hepatocellular carcinoma (HCC).Methods:We used small interfering RNA of MALAT1 (si-MALAT1) to knockdown MALAT1 in HuH-7. At the meanwhile, cells which were transfected with si-NC were used as the negative control group. Expression of NEAT1, cell proliferation and invasion function were detected these two groups. HuH-7 cells were transfected with lentivirus NEAT1 over expressing vector (lv-NEAT1) or negative control (lv-control). Expression of exosomes secretion related genes were analyzed between lv-NEAT1 and lv-control groups. Cells of lv-NEAT1 were knockdown MALAT1 expression using si-MALAT1, which could be si-MALAT1+ lv-NEAT1 group. exosomes secretion was detected in si-NC, si-MALAT1 and si-MALAT1+ lv-NEAT1 group. We treated cells (si-MALAT1 group) with exosomes from cells with lv-NEAT1 or lv-control to divide cells as si-MALAT1+ exosomes of lv-NEAT1 cells and si-MALAT1+ exosomes of lv-control groups. Cell proliferation and invasion of cells were detected in two groups.Results:Low expression of NEAT1 were found in MALAT1 knockdown cells compared with si-NC group [(0.72±0.02) vs. (0.98±0.01), P<0.05]. Cells with MALAT1 knockdown shown diminished proliferation [(0.66±0.03) vs. (0.98±0.04), P<0.05)] and invasion [(88.33±7.26) vs. (147.70±13.62), P<0.05)]. Compared with si-NC group, CD9 and CD63 expression were decreased in exosomes of si-MALAT1 group. Compared with si-MALAT1 group, CD9 and CD63 expression was increased in exosomes of si-MALAT1+ lv-NEAT1 group. Compared with si-MALAT1+ exosomes of lv-control group, proliferation [(0.97±0.03) vs. (0.74±0.05), P<0.05)] and invasion [ (132.70±7.36) vs. (98.33±6.01), P<0.05) ] were increased in si-MALAT1+ exosomes of lv-NEAT1 group. Exosomes related genes expression including HSPA8 (5.53±0.31), SLC3A2 (0.32±0.07) and SLC7A5 (0.77±0.45) were changed in lv-NEAT1 group compared with lv-control group [(0.98±0.15), P<0.05]. Conclusion:MALAT1 induced exosomes secretion by NEAT1 and exosomes related genes regulation. This regulation might be related with increased proliferation and invasion function in HCC cells with MALAT1 and NEAT1 abnormal expression.
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Background Arsenic is a toxicant that can affect the expressions of the cellular anti-apoptotic gene BCL-2 and its protein, but the effects of arsenic on BCL-2α and BCL-2\begin{document}$\beta $\end{document} transcripts have not been reported. Objective To investigate the potential effects of arsenic and its metabolites, methylarsonic acid (MMA) and dimethylarsonic acid (DMA), on BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T (total of α and \begin{document}$\beta $\end{document} transcripts) in human bronchial epithelial cells (16HBE) and human lung adenocarcinoma cells (A549). Methods 16HBE cells and A549 cells were randomly divided into three categories of exposure after in vitro culture: single-selected arsenic compound exposure groups with isoconcentration (16HBE cells were treated with 4.5 μmol·L−1 of MMA, DMA, and sodium arsenite, respectively, while A549 cells were treated with 60 μmol·L−1 of MMA, DMA, and sodium arsenite, respectively), sodium arsenite exposure groups with different concentrations (16HBE cells were treated with 1.5, 3.0, and 4.5 μmol·L−1 of sodium arsenite respectively, while A549 cells were treated with 20, 40, and 60 μmol·L−1 of sodium arsenite respectively), and combined exposure groups (i.e. MMA+sodium arsenite, and DMA+sodium arsenite; the exposure concentrations of 16HBE cells were both 1.5 μmol·L−1 and both 4.5 μmol·L−1 respectively, and those of A549 cells were both 20 μmol·L−1 and both 60 μmol·L−1 respectively). Meanwhile, a blank control group was also set up in each exposure category. After 48 h of continuous exposure, the relative expressions of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T in both cells were detected by real-time PCR. Results Regarding the single-selected arsenic compound exposure, in 16HBE cells, the expression levels of BCL-2α and BCL-2T under 4.5 μmol·L−1 MMA treatment were lower than those in their control groups (q=3.27, 2.93, both P<0.05), and the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T under 4.5 μmol·L−1 sodium arsenite were lower than those in their respective control groups (q=11.06, 3.65, 10.70, all P<0.05). In A549 cells, the expression level of BCL-2T treated with 60 μmol·L−1 DMA was lower than that in the control group (q=3.12, P<0.05), and the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T treated with 60 μmol·L−1 sodium arsenite were lower than those in their respective control groups (q=7.59, 7.27, 8.06, all P<0.05). Regarding the sodium arsenite exposure: 16HBE cells treated with 1.5 μmol·L−1 sodium arsenite had a lower expression level of BCL-2α and a higher expression level of BCL-2\begin{document}$\beta $\end{document} than those in their respective control groups (q=6.06, 11.92, both P<0.05); the expression level of BCL-2α under 3.0 μmol·L−1 sodium arsenite was lower than that in the control group (q=12.72, P<0.05); and under 4.5 μmol·L−1 sodium arsenite treatment, the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T were lower than those in their respective control groups (q=15.72, 6.79, 6.62, all P<0.05). The expression levels of BCL-2α gradually decreased with increasing concentrations of sodium arsenite (Fα trend=144.80, P<0.001), while BCL-2\begin{document}$\beta $\end{document} and BCL-2T decreased in a dose-dependent manner in the range of 1.5-4.5 μmol·L−1 (F\begin{document}${}_{\beta } $\end{document} trend=135.40, FT trend=38.24, both P<0.001). In A549 cells, the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T under each concentration of sodium arsenite treatments were lower than those in their respective control groups (all P<0.05); the results of further trend tests showed that their expression levels gradually decreased with increasing concentrations of sodium arsenite (Fα trend =31.97, F\begin{document}${}_{\beta} $\end{document} trend=549.50, FT trend=252.40, all P<0.001). Regarding the combined exposure, under MMA+sodium arsenite treatment at both 60 μmol·L−1, the expression levels of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T in A549 cells were higher than those in their respective control groups (q=6.37, 14.91, 5.33, all P<0.05); under DMA+sodium arsenite treatment at both 60 μmol·L−1, their expression levels in A549 cells were also higher than those in their respective control group (q=8.60, 17.29, 6.91, all P<0.05). Conclusion Exposure to a high concentration (16HBE: 4.5 μmol·L−1, A549: 60 μmol·L−1) of a single arsenic metabolite has no effect on BCL-2 transcripts in 16HBE cells and A549 cells. Exposure to a low concentration (1.5 μmol·L−1) of sodium arsenite alone would decrease the expression level of BCL-2α and increase the expression level of BCL-2\begin{document}$\beta $\end{document} in 16HBE cells, and exposure to all designed concentrations of sodium arsenite alone would decrease the expressions of all transcripts in A549 cells. The combined exposure to high concentrations (both 60 μmol·L−1) of MMA plus sodium arsenite or high concentrations (both 60 μmol·L−1) of DMA plus sodium arsenite would increase the expressions of BCL-2α, BCL-2\begin{document}$\beta $\end{document}, and BCL-2T in A549 cells, which are different from the effects presented by single exposure.
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@#Metastasis-associated lung adenocarcinoma transcript 1(MALAT1)is one of the first identified LncRNA associated with human diseases. Unlike most members of the LncRNA family, MALAT1 is found in almost all human tissues and expressed at a relatively high level. At present, MALAT1 is known to play a vital role in the pathophysiological process of many diseases such as tumors, cardiovascular diseases, and nervous system diseases. In recent years, studies have found that MALAT1 may be involved in many ocular diseases(such as diabetic retinopathy, cataracts, glaucoma, retinoblastoma, neonatal retinopathy, <i>etc</i>.)play an important role in the pathological development process, and it is expected to become an effective target for the diagnosis and treatment of eye diseases. This article summarizes the research progress of eye diseases in which MALAT1 has participated in recent years.
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Objective:To evaluate the effects of berberine on necroptosis of non-alcoholic fatty liver disease in mice and its relationship with adenosine monophosphate-activated protein kinase(AMPK)/ signal transducer and activator of transcription 6(STAT6) pathway.Methods:Twenty-five 8-week-old male C57BL/6N mice were divided into control group, steatotic liver group, berberine treatment group(200 mg·kg -1·d -1), AMPK inhibitor Compound C treatment group(0.2 mg·kg -1·d -1), and STAT6 inhibitor AS1517499 treatment group(10 mg·kg -1·d -1). After 12 weeks of intervention, the mice and liver tissue were weighed, and serum aspartate aminotransferase(AST), alanine aminotransferase(ALT), triglyceride, tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β) as well as liver malondialdehyde and superoxide dismutase were measured; liver tissue HE, Masson, and oil red O staining were performed. Western blotting was used to detect the expressions of necroptosis related proteins[receptor interaction protein kinase 3(RIPK3), phosphorylated(p-) mixed lineage kinase domain-like(MLKL)], AMPK, p-AMPK, and p-STAT6. Results:Compared with control group, the steatotic liver group had higher quality of liver and liver index, and higher levels of serum AST, ALT, triglyceride, TNF-α, IL-1β, and oxidative stress( P<0.05); Liver tissue was full of cavity changes and inflammatory cell infiltration, widely distributed red lipid droplets and obvious blue fiber dyeing; The expressions of RIPK3 and p-MLKL were up-regulated ( P<0.05), but the levels of p-AMPK and p-STAT6 were relatively reduced ( P<0.05). Compared with the steatotic liver group, berberine intervention decreased liver quality and liver index, improved liver function, reduced blood lipid levels, pro-inflammatory factor expression and oxidative stress level, and significantly alleviated the degree of liver steatosis and fibrosis, the levels of RIPK3 and p-MLKL ( P<0.05), while the expressions of p-AMPK and p-STAT6 were increased significantly ( P<0.05). As compared with the berberine treatment, AMPK and STAT6 inhibitor treatment could offset the protective effect of berberine on steatotic liver, moreover, the expressions of RIPK3 and p-MLKL were increased ( P<0.05). There was no statistical difference in AMPK total protein content among the five groups ( P>0.05). Conclusion:Berberine can activate AMPK/STAT6 pathway to inhibit the necroptosis of hepatocyte, thus plays a protective role on non-alcoholic fatty liver disease in mice.
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The occurrence and development of breast cancer is a complicated process, in which many kinds of bioactive substances are involved. As a long non-coding RNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) not only plays a role in multiple sites of breast cancer, but also plays an important role in the treatment and prognosis evaluation of breast cancer patients. This article reviews the research progress of MALAT1 in breast cancer.