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1.
J Cell Mol Med ; 2021 Jan 23.
Artigo em Inglês | MEDLINE | ID: mdl-33484498

RESUMO

Hepatocellular carcinoma (HCC) is one of the most common cancers with high prevalence and mortality, and it has brought huge economic and health burden for the world. It is urgent to found novel targets for HCC diagnosis and clinical intervention. Circular RNA (circRNA) has been reported to participate in many cancer progressions including HCC, suggesting that circRNA might paly essential role in HCC initiation and progression. Our study aims to found that potential circRNA participates in HCC development and its underlying molecular mechanisms. We obtained three pairs of HCC tissues and its adjacent normal tissues data from GEO DataSets. MTT, cell colony, EdU, wound-healing, transwell invasion and mouse xenograft model assays were used to demonstrate the biological functions of circCAMSAP1 in HCC progression. Furthermore, we conducted bioinformatics analysis, AGO2-RIP, RNA pull-down and luciferase reporter assays to assess the association of circCAMSAP1-miR-1294-GRAMD1A axis in HCC cells. The expression of circCAMSAP1 was up-regulated in HCC tissues compared with its adjacent normal tissues. Up-regulation of circCAMSAP1 promoted HCC biological functions both in vitro and in vivo. The promotive effects of circCAMSAP1 on HCC progression function through miR-1294/GRAMD1A pathway. CircCAMSAP1 was up-regulated in HCC tissues, and circCAMSAP1 up-regulated GRAMD1A expression to promote HCC proliferation, migration and invasion through miR-1294. CircCAMSAP1 might be a potential prognosis and therapeutic target for HCC.

2.
Cancer Med ; 10(3): 833-842, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33481351

RESUMO

Increasing circRNAs have attracted a lot of attention because of their significant biological effects in many diseases. It has been reported that circ_0008305 can modulate lung cancer progression. However, the association between circ_0008305 and hepatocellular carcinoma (HCC) needs to be well explored. In this current research, we studied the molecular function and potential mechanism of circ_0008305 in HCC progression. First, it was demonstrated that circ_0008305 was greatly increased in HCC tissues and cells. Moreover, we observed silencing circ_0008305 markedly repressed HCC cells in vitro growth and reduced tumor growth in vivo. Additionally, it was identified that circ_0008305 can act as a sponge of miR-660 while miR-660 targeted Bcl-2-associated athanogene 5 (BAG5). BAG5 belongs to a member of BAG family and it is involved in multiple diseases. We reported that circ_0008305 contributed to the inhibition of miR-660, which resulted in an upregulated expression of BAG5 in HCC. Subsequently, rescue assays were conducted and it was indicated that loss of BAG5 reversed the effects of miR-660 inhibitors on HCC partially. To sum up, it was illustrated by our study that circ_0008305-mediated miR-660-5p/BAG5 axis triggered HCC progression, which could provide a novel insight on the underlying mechanism of HCC progression.

3.
J Immunol Res ; 2020: 8873261, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33294469

RESUMO

Stroke is a cerebrovascular disease that results in decreased blood flow. Although Panax notoginseng (PN), a Chinese herbal medicine, has been proven to promote stroke recovery, its molecular mechanism remains unclear. In this study, middle cerebral artery occlusion (MCAO) was induced in rats with thrombi generated by thread and subsequently treated with PN. After that, staining with 2,3,5-triphenyltetrazolium chloride was employed to evaluate the infarcted area, and electron microscopy was used to assess ultrastructural changes of the neurovascular unit. RNA-Seq was performed to determine the differential expressed genes (DEGs) which were then verified by qPCR. In total, 817 DEGs were identified to be related to the therapeutic effect of PN on stroke recovery. Further analysis by Gene Oncology analysis and Kyoto Encyclopedia of Genes and Genomes revealed that most of these genes were involved in the biological function of nerves and blood vessels through the regulation of neuroactive live receptor interactions of PI3K-Akt, Rap1, cAMP, and cGMP-PKG signaling, which included in the 18 pathways identified in our research, of which, 9 were reported firstly that related to PN's neuroprotective effect. This research sheds light on the potential molecular mechanisms underlying the effects of PN on stroke recovery.

4.
Medicine (Baltimore) ; 99(50): e23542, 2020 Dec 11.
Artigo em Inglês | MEDLINE | ID: mdl-33327303

RESUMO

BACKGROUND: We performed a meta-analysis to more precisely evaluate the association between the cytotoxic T lymphocyte-associated protein 4 (CTLA-4) -1772T/C polymorphism and overall gastric cancer (GC) risk and the influence of ethnicity and the source of controls on that association. METHODS: A systematic literature search was performed in PubMed, EMBASE, the Cochrane Library, Web of Science (WOS) Database, Chinese National Knowledge Infrastructure (CNKI), China biomedical literature database (CBM), Wanfang database, and VIP. Two investigators independently reviewed the articles, and disagreements were resolved by discussion and consensus. The odds ratio (OR) with 95% confidence intervals (CIs) was used to assess the strength of the association between the CTLA-4 -1722T/C polymorphism and GC risk, based on the genotype frequencies in cases and controls. The meta-analyses were performed with Stata 12.0, using two-sided P values. Trial sequential analysis (TSA) was calculated by TSA Software. RESULTS: Overall, we identified 5 studies including 1039 GC cases and 2136 controls that evaluated the association of the CTLA-4 -1722T/C polymorphism and GC risk. Overall, there was no significant association between the CTLA-4-1722T/C polymorphism and the risk of GC. In the subgroup analysis based on ethnicity, the results showed that the relationship between the CTLA-4 -1722T/C polymorphism and GC susceptibility was strongest in the Chinese population rather than in the Iranian population (TC vs CC: OR = 1.405, 95% CI: 1.100-1.796, P = .007; TC+TT vs CC: OR = 1.329, 95% CI: 1.052-1.680, P = .017). Then, there was a significant association between the CTLA-4 -1722T/C polymorphism and the risk of GC in studies with HB controls. However, the above correlation can only be reflected in specific populations and gene models. Therefore, we believe that the evidence of this correlation is insufficient. CONCLUSION: Our meta-analysis showed that the CTLA-4 -1722T/C polymorphism may be associated with the susceptibility to GC. However, the slight correlation can only be reflected in specific populations and gene models. Therefore, we believe that this association is negligible. The large and well-designed case-control studies are needed to validate our findings.


Assuntos
Antígeno CTLA-4/genética , Neoplasias Gástricas/genética , Predisposição Genética para Doença/genética , Humanos , Polimorfismo de Nucleotídeo Único/genética
6.
Front Oncol ; 10: 578816, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33224879

RESUMO

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in China. N6-methyladenosine (m6A) plays an important role in posttranscriptional gene regulation. METTL3 and IGF2BP2 are key genes in the m6A signal pathway and have recently been shown to play important roles in cancer development and progression. In our work, higher METTL3 and IGF2BP2 expression were found in HCC tissues and were associated with a poor prognosis. In addition, IGF2BP2 overexpression promoted HCC proliferation in vitro and in vivo. Mechanistically, IGF2BP2 directly recognized and bound to the m6A site on FEN1 mRNA and enhanced FEN1 mRNA stability. Overall, our study revealed that METTL3 and IGF2BP2, acting as an oncogene, maintained FEN1 expression through an m6A-IGF2BP2-dependent mechanism in HCC cells, and indicated a potential biomarker panel for prognostic prediction in liver cancer.

7.
Anal Chim Acta ; 1139: 42-49, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-33190708

RESUMO

We have developed a versatile label-free surface-enhanced Raman spectroscopic platform for detecting various biotargets via proximity hybridization-triggered DNA assembly based on the 736 cm-1 Raman peak of adenine breathing mode. We initially immobilized the first probe to AuNPs and modified the second with poly adenine. Presence of target DNA or protein molecules assembled a sandwich complex that brought the poly adenine close to the AuNPs surface, generating Raman signals, that were proportional to target molecule concentration. These approach exhibits high sensitivity, with a detection limit of 5.4 pM, 47 fM, and 0.51 pg/mL for target DNA, thrombin and CEA, respectively. Owing to a one step proximity dependent complex formation, this technique is simple and can be completed within 40 min, making it a promising candidate for point-of-care testing applications.

8.
Front Genet ; 11: 1029, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33193591

RESUMO

Recent studies have investigated the modulatory roles of long non-coding RNAs in the onset and progression of liver cancer. The present study aimed to elucidate the role of lnc-GNAT1-1 in liver cancer development and to explore the underlying mechanisms. Quantitative real-time polymerase chain reaction was performed to measure the expression levels of lnc-GNAT1-1 in cancerous tissues from patients with liver cancer and in liver cancer cell lines. The proliferative ability and apoptotic rates of liver cancer cells were measured using the counting kit-8 (CCK-8), colony formation, and flow cytometry assays. The abilities to invade and migrate were measured using Transwell assays. Epithelial-mesenchymal transition (EMT)-related proteins, E-cadherin, N-cadherin, and vimentin, were measured using western blotting. A nude mouse model was injected with xenografts to evaluate tumor growth in vivo. Downregulation of lnc-GNAT1-1 was observed in cancerous tissues from patients with liver cancer and in liver cancer cell lines, and low expression levels of lnc-GNAT1-1 were related to advanced TNM stage. Lnc-GNAT1-1 knockdown promoted invasion, migration, and proliferation of liver cancer cells and inhibited apoptosis, while lnc-GNAT1-1 upregulation exerted the opposite effects. The expression levels of lnc-GNAT1-1 negatively correlated with in vivo tumor growth in a xenograft nude mouse model. Mechanistic experiments revealed that lnc-GNAT1-1 exerted anti-tumor effects in liver cancer cells by inhibiting EMT. In conclusion, this study suggests that lnc-GNAT1-1 suppresses liver cancer progression by modulating EMT.

9.
Onco Targets Ther ; 13: 9203-9211, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32982307

RESUMO

Introduction: In East Asia, hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancer types. Long noncoding RNA (lncRNA) prostate androgen-regulated transcript 1 (PART1) was reported to play crucial roles in regulating cancer progression. However, roles and mechanisms of action of PART1 in hepatocellular carcinoma (HCC) still remain unknown. Methods: Quantitative real-time polymerase chain reaction (RT-qPCR) method was used to detect the PART1 expression level in HCC cells. Cell proliferation, colony formation, and transwell invasion assays were performed to investigate the biological roles of PART1 on HCC cell behaviors. Bioinformatic analysis methods were performed to analyze connections of microRNA-590-3p (miR-590-3p) with PART1 or high mobility group box 2 (HMGB2) in HCC. Moreover, expression levels of PART1, miR-590-3p, and HMGB2 in HCC tissues and normal tissues were analyzed at ENCORI. Results: PART1 expression was found to be significantly upregulated in HCC tissues and cells. Functionally, silencing of PART1 significantly suppressed HCC cell proliferation, colony formation and invasion in vitro, while forcing PART1 exerts opposite biological effects. Mechanically, miR-590-3p/HMGB2 axis was downstream target of PART1, and silencing of miR-590-3p or forcing of HMGB2 could rescue the stimulation effects of PART1 overexpression on HCC cell behaviors. Discussion: Our results provided evidence that PART1 serves as oncogenic lncRNA through sponging miR-590-3p to upregulate HMGB2 expression in HCC.

10.
Cancer Med ; 9(19): 7125-7136, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32810392

RESUMO

Hepatocellular carcinoma (HCC) is an aggressive malignancy with limited effective treatments and ranks as the second most lethal tumor. Immunotherapy has brought great hope for HCC treatment. Oxysophocarpine is a bioactive alkaloid which poses various pharmacological functions including neuroprotective, anti-virus, anti-convulsant, and anti-nociception. However, there is little systematic study of Oxysophocarpine against HCC and its underlying potential and mechanism combined with immunotherapy in HCC treatment remain poorly unknown. This study was aimed to investigate whether Oxysophocarpine can distinctly suppress HCC cells and sensitize the immunotherapy of CD8+ T cells against HCC. We used HepG2, Hepa1-6, and primary CD8+ T cells to perform in vitro assays and Hepa1-6 subcutaneous tumor to conduct in vivo assay. Oxysophocarpine inhibited the proliferation and increased the apoptosis of HepG2 and Hepa1-6 cells, meanwhile suppressed the migration of HepG2 and Hepa1-6 cells. Oxysophocarpine sensitized the Lag-3 immunotherapy effect of CD8+ T cells against HCC in vivo and in vitro by decreasing Fibrinogen-like protein 1 (FGL1) expression through downregulating IL-6-mediated JAK2/STAT3 signaling, whereas Oxysophocarpine treatment had a little effect of CD8+ T cells cytotoxicity function against HCC with PD-1, Tim-3, or TIGIT blockade. Our studies provided preclinical basis for clinical application of Oxysophocarpine.

11.
Am J Transl Res ; 12(5): 2192-2200, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32509211

RESUMO

Emerging evidence demonstrated long non-coding RNA (lncRNA) small nucleolar RNA host gene 5 (SNHG5) participates in the tumorigenesis. The aim of this work was to characterize the expression and biology roles of SNHG5 in hepatocellular carcinoma (HCC). Expression level of SNHG5 in HCC cells was analyzed with RT-qPCR. Cell proliferation rate, cell cycle distribution, and cell migration ability was analyzed with cell counting kit-8 assay, flow cytometry, and wound-healing assay, respectively. Targets prediction were performed at LncBase V2.0 and TargetScan. SNHG5 was found elevated expression in HCC cell lines. In vitro functional experiments showed knockdown of SNHG5 inhibits cell proliferation and migration, while overexpression of SNHG5 exerted opposite effects. Mechanism studies showed SNHG5 functions as competitive endogenous RNA (ceRNA) for microRNA-23c (miR-23c) to promote high mobility group box 2 (HMGB2) expression. miR-23c was downregulated, while HMGB2 was upregulated in HCC tissues and cells. We revealed SNHG5 could exert an oncogenic role in HCC via regulating miR-23c/HMGB2 axis. Targeting SNHG5 might be a novel therapeutic measure to suppresses HCC progression.

12.
Biosci Rep ; 40(5)2020 05 29.
Artigo em Inglês | MEDLINE | ID: mdl-32400857

RESUMO

AIM: To investigate the relationship between PI3K/Akt/NF-κB cellular signal pathway and the expression of P-gp and LRP in multidrug resistance (MDR) cell of nasopharyngeal carcinoma. METHOD: The PI3K, p-Akt and NF-κB/p65 as the activity of PI3K/Akt/NF-κB were detected by Western blot. The expressions of LRP and P-gp were detected by Western blot and real-time PCR. RESULT: The RIs of CNE/DDP group to DDP, 5-Fu, VCR, ADR and PTX were 35.04, 18.14, 24.13, 12.00 and 10.18, respectively. The RIs of LY-294002 group were 11.77, 5.83, 3.07, 3.86 and 3.34, and PDTC group were 11.08, 6.55, 7.66, 2.18 and 4.05. The expressions of PI3K, p-Akt and NF-κBp65, LRP and P-gp were increased and mRNA of LRP and P-gp were up-regulated in CNE/DDP. The expression of p-Akt in LY-294002 group was down-regulated. The expression of NF-κB p65 in PDTC group was decreased. The mRNA of LRP and P-gp in LY-294002 group and PDTC group were decreased. CONCLUSION: MDR of nasopharyngeal carcinoma cell can be regulated by activating PI3K/Akt/NF-κB signal pathway and then increase the expression of P-gp and LRP. The MDR of nasopharyngeal carcinoma cell can be reversed by inhibiting PI3K/Akt/NF-κB signal pathway.

13.
Oncol Res ; 2020 May 29.
Artigo em Inglês | MEDLINE | ID: mdl-32471520

RESUMO

There is growing evidence on the clinical significance of Tumor Microenvironment (TME) cells in predicting prognosis and therapeutic effects. However, cell interactionsin tumor microenvironments have not been thoroughly studied or systematicallyanalyzed so far. In this study, 22 immune cell components in the lung adenocarcinoma(LUAD) TME were analyzed using gene expression profile from The Cancer GenomeAtlas (TCGA), Gene Expression Omnibus (GEO) . The TME based molecular subtypesof LUAD were defined to evaluate further the relationship between molecular subtypes,prognosis, and clinical characteristics. A TME risk score model was constructed byusing the differentially expressed genes (DEGs) of molecular subtypes. The relationshipbetween the TME score and clinical characteristics and genomic mutations wascompared to identify the genes that have significant associations with the TME. Thecomprehensive analysis of the TME characteristics maybe helpful in revealing theresponse of LUAD patients to immunotherapy, providing a new strategy forimmunotherapy.

14.
Pathol Res Pract ; 216(3): 152828, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32008867

RESUMO

Recent researches indicated Ddx5 and Ddx17 play crucial roles in tumorigenesis. However, the study of Ddx5 and Ddx17 in glioma remains a little. Our study investigated their expression in glioma and evaluated its association with clinical factors and prognostic significance. The expression of Ddx5 and Ddx17 were both upregulated in glioma tissues compared to normal brain tissues, and a significant positive correlation between Ddx5 and Ddx17 expression was identified by statistical analysis. Immunohistochemical staining verified the expression of Ddx5 and Ddx17 in peritumoral zone was lower than that in core zone but higher than normal brain tissues. Moreover, the increased expression of Ddx5 and Ddx17 was markedly correlated with WHO Grade and histological type, and high Ddx5 and Ddx17 were found to be significantly associated with the worse overall survival of glioma patients. In additional, higher expression of both Ddx5 and Ddx17 predicted shorter clinical survival time for high-grade glioma patients with radiotherapy or with chemotherapy. In conclusion, overexpressed Ddx5 and Ddx17 are involved in the clinical progression and poor prognosis of glioma patients, suggesting that their upregulation can be used as a reliable clinical predictor for tumor diagnosis and to predict survival in patients with glioma.


Assuntos
Biomarcadores Tumorais/metabolismo , Neoplasias Encefálicas/patologia , RNA Helicases DEAD-box/biossíntese , Glioma/patologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Neoplasias Encefálicas/enzimologia , Neoplasias Encefálicas/mortalidade , Progressão da Doença , Feminino , Glioma/enzimologia , Glioma/mortalidade , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Regulação para Cima , Adulto Jovem
15.
Aging (Albany NY) ; 12(24): 26236-26247, 2020 12 26.
Artigo em Inglês | MEDLINE | ID: mdl-33401249

RESUMO

Exosomes are small vesicles with a diameter of 30-150 nm secreted by cells, which can be used as signal carriers to transfer nucleic acids, proteins, lipids and other functional substances to the recipient cells and play a role in cell communication. Hepatocellular carcinoma is the fourth most common cause of cancer-related death worldwide. Studies have shown that long non-coding RNAs (lncRNAs) are involved in the development and progression of many types of tumors. Our present study found that linc-FAM138B was reduced in HCC tissues and cell lines, low expression of linc-FAM138B indicated a poor prognosis in HCC patients. Interestingly, linc-FAM138B could be packaged into cancer cells. And exo-FAM138B inhibited the proliferation, migration and invasion of HCC cells. Furthermore, linc-FAM138B sponged miR-765 levels. And exo-si-FAM138B promoted HCC progression, while deletion of miR-765 reversed the role of exo-si-FAM138B. In vivo tumorigenesis experiments showed that exo-FAM138B suppressed HCC growth via modulating miR-765. In conclusion, exo-linc-FAM138B secreted by cancer cells inhibited HCC development via targeting miR-765, which provided a new idea and perspective for in-depth understanding of the complex signal regulation in HCC process.

16.
Biomed Pharmacother ; 120: 109551, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31648164

RESUMO

OBJECTIVES: Emerging microRNAs (miRNAs) are validated to take part in pathological processes, including numerous carcinomas. Currently, we focused on the functional role of miR-383 and interleukin-17 (IL-17) in hepatocellular carcinoma (HCC), and the underlying molecular mechanisms were also the emphases in our research. METHODS: We used reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to measure the expression levels of miR-383 in 45 paired tumor tissues and adjacent non-tumor tissues extracted from patients with hepatocellular carcinoma. These tissues were also stained for IL-17 using immunohistochemical staining. Western blot was performed to detect the protein expressions of following protein-coding genes, including p-Stat3, Stat3 and GAPDH. A dual-luciferase activity was carried out to determine whether IL-17 was the downstream gene of miR-383 in hepatocellular carcinoma development. The colony assay, CCK8 assay, and apoptosis assay were used to explore the detailed regulatory effects of miR-383/IL-17 axis in the cellular processes of hepatocellular carcinoma separately. RESULTS: miR-383 was down-regulated significantly in tumor tissues, while IL-17 was up-regulated. IL-17 was certificated to act as the downstream gene of miR-383. Furthermore, overexpression of miR-383 suppressed cell proliferation and promoted apoptosis in hepatocellular carcinoma. However, the raised IL-17 attenuated the inhibition effect of miR-383 in hepatocellular carcinoma. In addition, we found that p-Stat3 was repressed by miR-383, and the up-regulation of IL-17 reversed the suppression effect in hepatocellular carcinoma. CONCLUSIONS: miR-383 may play a anti-tumor role in the pathogenesis of hepatocellular carcinoma by targeting IL-17 through STAT3 signaling pathway. miR-383/IL-17 axis maybe a potent target for the clinical diagnosis and treatment of hepatocellular carcinoma.


Assuntos
Apoptose , Carcinoma Hepatocelular/patologia , Interleucina-17/metabolismo , Neoplasias Hepáticas/patologia , MicroRNAs/metabolismo , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais , Apoptose/genética , Sequência de Bases , Carcinoma Hepatocelular/genética , Linhagem Celular Tumoral , Proliferação de Células/genética , Regulação para Baixo/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Hepáticas/genética , MicroRNAs/genética , Fosforilação , Regulação para Cima/genética
17.
Nan Fang Yi Ke Da Xue Xue Bao ; 39(8): 911-916, 2019 Aug 30.
Artigo em Chinês | MEDLINE | ID: mdl-31511210

RESUMO

OBJECTIVE: To investigate the effect of curcumin on the invasion and migration of human glioma cells in vitro and explore the molecular mechanisms. METHODS: MTT assay was used for screening the optimal curcumin concentrations. The effects of curcumin on the invasion and metastasis of human glioma cell lines U251 and LN229 were tested using Transwell assay, Boyden assay and wound-healing assays. The expression of the related proteins and their interactions were determined using Western blotting and coimmunoprecipitation assay. RESULTS: Curcumin at the concentration of 20 µmol/L for 48 h was used as the optimal condition for subsequent cell treatment. In the two glioma cell lines, curcumin significantly suppressed the invasion and migration of the cells (P < 0.05) and lowered the expressions of hepatoma-derived growth factor (HDGF), Ncadherin, vimentin, Snail and Slug, but increased the expression of E-cadherin. Interference of HDGF in curcumin-treated glioma cells synergistically inhibited the epithelial-mesenchymal transition (EMT) signals, while overexpression of HDGF significantly reversed the inhibitory effect of curcumin on EMT; curcumin treatment could significantly reduce the binding of HDGF to ß-catenin. CONCLUSIONS: Curcumin suppresses EMT signal by reducing HDGF/ß-catenin complex and thereby lowers the migration and invasion abilities of human glioma cells in vitro.


Assuntos
Glioma , Linhagem Celular Tumoral , Movimento Celular , Curcumina , Transição Epitelial-Mesenquimal , Humanos , Peptídeos e Proteínas de Sinalização Intercelular , Invasividade Neoplásica , beta Catenina
18.
J Cell Biochem ; 120(11): 18816-18825, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31297882

RESUMO

Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world. Nevertheless, its underlying molecular mechanisms are largely unknown. LINC00152 are recently investigated in several cancer types. In our current investigation, we observed LINC00152 was obviously upregulated in HCC cells. LINC00152 was significantly downregulated by infecting LV-shLINC00152 in HepG2 and SNU449 cells. Loss of LINC00152 remarkably repressed HCC cell proliferation, cell colony formation, induced cell apoptosis, and restrained cell migration/invasion. Growing evidence has reported long noncoding RNAs can sponge microRNAs to modulate cancer process. Here, we indicated miR-215 was greatly decreased in HCC and LINC00152 regulated HCC development via sponging miR-215. For another, the binding association between LINC00152 and miR-215 was proved by a series of functional assays. CDK13 was predicted as the target of miR-215. Upregulation of miR-215 greatly depressed CDK13 in HCC cells. Subsequently, the in vivo results demonstrated that silence of LINC00152 restrained HCC development via modulating miR-215 to up-regulate CDK13. Therefore, it was revealed that LINC00152 contributed to the progression of HCC by the modulation of miR-215 and CDK13.


Assuntos
Proteína Quinase CDC2/metabolismo , Carcinoma Hepatocelular/metabolismo , Neoplasias Hepáticas/metabolismo , MicroRNAs/metabolismo , Proteínas de Neoplasias/metabolismo , RNA Longo não Codificante/metabolismo , RNA Neoplásico/metabolismo , Transdução de Sinais , Animais , Proteína Quinase CDC2/genética , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Células Hep G2 , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Camundongos , Camundongos Endogâmicos BALB C , MicroRNAs/genética , Proteínas de Neoplasias/genética , RNA Longo não Codificante/genética , RNA Neoplásico/genética
19.
Wei Sheng Yan Jiu ; 48(3): 418-422, 2019 May.
Artigo em Chinês | MEDLINE | ID: mdl-31133127

RESUMO

OBJECTIVE: To investigate the effect of two-year nutritional intervention on the body composition in Yao primary school students in Guangxi Zhuang Autonomous Region. METHODS: Four primary schools in towns mainly inhabited by Yao People in Jinxiu Yao Autonomous County of Guangxi Zhuang Autonomous Region were chosen randomly as the intervention schools, from which one class was randomly chosen per grade from grades 2-4(7-12 years old); Four other primary schools with similar economic and social conditions to the intervention schools were chosen as the control schools. In total, 190 and 146 students were included in the intervention group and the control group, respectively. The control group gave basic food allowance and the intervention group gave milk and eggs on this basic. Students in the intervention group were subject to nutritional intervention. The change in body composition of students of different body weights was observed and analyzed at the baseline time(September 2015; T0), and 1(T1) and 2(T2) years after intervention. The mixed linear model was used to analyze repeated measures data, and multivariate ANOVA was performed. RESULTS: No significant differences existed in all indexes for both boys and girls between the two groups at T0(P > 0.05). At T1 and T2, as compared with the control group, the fat-free body weight(χ~2=7.253, P<0.05), body fat(χ~2=6.181, P<0.05; χ~2=5.226, P<0.05) and body fat percentage(χ~2=4.284, P<0.05; χ~2=2.227, P<0.05) of boys, and the fat-free body weight(χ~2=3.287, P<0.05; χ~2=2.788, P<0.05) and body fat(χ~2=3.261, P<0.05; χ~2=2.135, P<0.05) of girls increased significantly in the intervention group. The fat-free body weight(χ~2=5.381, P<0.05; χ~2=3.278, P<0.05) and body fat(χ~2=5.987, P<0.05; χ~2=3.921, P<0.05) in both the intervention and the control groups increased significantly at T1 and T2 as compared with T0. Multivariate ANOVA result showed that, the fat-free body weight and body fat were significantly different between different time periods after age, height and body weight were controlled for boys but not girls. When body weights of different levels were included, the fat-free body weight(χ~2=6.234, P<0.05; χ~2=4.076, P<0.05) and body fat(χ~2=5.479, P<0.05; χ~2=2.315, P<0.05) increased significantly in low-, middle-and high-level subgroups of the intervention group at T1 and T2 as compared with the control group. The fat-free body weight(χ~2=5.784, P<0.05; χ~2=3.679, P<0.05) and body fat(χ~2=4.783, P<0.05; χ~2=2.784, P<0.05) in low-, middle-and high-level subgroups of both the intervention and the control groups increased significantly at T1 and T2 as compared to those at T0(P<0.05). CONCLUSION: Nutritional intervention(including milk and eggs) can promote the change in body composition in boys in Jinxiu Yao Autonomous County primary schools of Guangxi Zhuang Autonomous Region, but produces not too much benefit for girls.


Assuntos
Composição Corporal , Instituições Acadêmicas , Peso Corporal , Criança , China , Cidades , Feminino , Humanos , Masculino , Estado Nutricional
20.
Int Immunopharmacol ; 73: 72-80, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31082725

RESUMO

In this research, we planned to dig the possible influences and mechanism of long noncoding (lnc) RNA HAGLROS in the development and progression of hepatocellular carcinoma (HCC). The levels of lncRNA HAGLROS in HCC tumor samples and their relationship with clinicopathological characteristics and prognosis of patients with HCC were studied. Subsequently, overexpression and silenced approaches were used in HCC cells for detecting the effects of lncRNA HAGLROS on cell viability, apoptosis, and autophagy. Furthermore, we investigated whether HAGLROS could function as a competing endogenous RNA (ceRNA) to regulate miR-5095 expression in HCC cells, and explored the correlation between miR-5095 and ATG12. Besides, the correlation of HAGLROS, the consequent PI3K/AKT/mTOR signaling pathway was further explored. The level of HAGLROS was higher in HCC tissues and correlated with clinical performances including tumor stages or tumor differentiation. In contrast to the lower level, a higher level of HAGLROS correlated with a shorter survival time of patients with HCC. The suppression of HAGLROS decreased cell viability, promoted apoptosis, and inhibited autophagy. Moreover, HAGLROS negatively regulated miR-5095 expression, which further regulated HCC cell viability, apoptosis, and autophagy. In addition, ATG12 was targeted by miR-5095 and was then involved in miR-5095-regulated HCC cell biological processes including viability, apoptosis, and autophagy. Furthermore, overexpression of HAGLROS activated PI3K/AKT/mTOR signals. Our results revealed that HAGLROS is highly expressed in HCC, and its high level may correlate with the progression and development of HCC involving the processes of cell viability, apoptosis, and autophagy through the miR-5095/ATG12 axis and PI3K/AKT/mTOR signals.


Assuntos
Proteína 12 Relacionada à Autofagia/genética , Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , MicroRNAs , RNA Longo não Codificante , Apoptose , Autofagia , Proteína 12 Relacionada à Autofagia/metabolismo , Carcinoma Hepatocelular/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Feminino , Humanos , Neoplasias Hepáticas/metabolismo , Masculino , Pessoa de Meia-Idade , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Serina-Treonina Quinases TOR/metabolismo
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