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Objective To investigate the relationship between the expression of miR-141-3p,miR-149-3p and proliferative genes,clinicopathological features and prognosis in endometrial carcinoma tissues.Methods From February 2017 to February 2019,98 patients with endometrial cancer were selected as the study objects.Real-time fluorescence quantitative PCR was used to detect the relative mRNA expression levels of miR-141-3p,miR-149-3p and proliferating genes[proliferating cell nuclear antigen(PCNA),cyclin D1,cyclin dependent kinase 4(CDK4)]in cancer tissues of patients with endometrial cancer.The correlation between the expres-sions of miR-141-3p,miR-149-3p and PCNA,cyclin D1 and CDK4 mRNA in cancer tissues of patients with en-dometrial cancer was analyzed by Pearson correlation analysis.The expression of miR-141-3p and miR-149-3p in cancer tissues of endometrial carcinoma patients with different clinicopathological characteristics was com-pared.Kaplan-Meier curve was used to analyze the influence of miR-141-3p and miR-149-3p expression on prognosis of patients with endometrial carcinoma.Univariate and multivariate Cox regression analysis of prog-nostic factors in patients with endometrial cancer.Results The relative expression levels of miR-141-3p,miR-149-3p,PCNA mRNA,cyclinD1 mRNA and CDK4 mRNA in cancer tissues of patients with endometrial carci-noma were higher than those in adjacent tissues,with statistical significance(P＜0.05).The expressions of miR-141-3p and miR-149-3p were positively correlated with the expressions of PCNA mRNA,cyclinD1 mR-NA and CDK4 mRNA in cancer tissues of patients with endometrial carcinoma(all P＜0.05).The relative ex-pression levels of miR-141-3p and miR-149-3p in cancer tissues of endometrial cancer patients with stage Ⅲand lymph node metastasis according to International Federation of Gynecology and Obstetrics(FIGO)were higher than those of endometrial cancer patients with stage Ⅰ-Ⅱ and no lymph node metastasis,respective-ly,and the difference was statistically significant(P＜0.05).The 3-year overall survival rate of miR-141-3p high expression group was significantly lower than that of miR-141-3p low expression group,and the differ-ence was statistically significant(Log-rank x2=7.043,P=0.008).The 3-year overall survival rate of patients with high miR-149-3p expression group was significantly lower than that of patients with low miR-149-3p ex-pression group,with statistical significance(Log-rank x2=7.094,P=0.007).FIGO stage Ⅲ,lymph node me-tastasis,miR-141-3p elevation and miR-149-3p elevation were independent risk factors for prognosis of pa-tients with endometrial cancer(P＜0.05).Conclusion Detecting the expression of miR-141-3p and miR-149-3p in cancer tissues of patients with endometrial carcinoma is helpful to evaluate the survival and prognosis of patients.
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BACKGROUND:Studies have shown that insulin-like growth factor 1/platelet-derived growth factor has an inhibitory effect on fibroblast apoptosis.miR-141-3p in bone marrow stromal cells increases with age and has a relationship with the activation of inflammatory signaling pathways,suggesting that it may be a therapeutic target for lumbar disc herniation. OBJECTIVE:To explore the effects of miR-141-3p on dorsal root ganglion inflammation and lower limb pain in rats with lumbar disc herniation by regulating insulin-like growth factor 1/platelet-derived growth factor. METHODS:Fifty male Sprague-Dawley rats,SPF level,were randomly divided into normal group,model group,miR-NC group,miR-141-3p inhibitor group and miR-141-3p mimics group,with 10 rats in each group.Except for the normal group,animal models of lumbar disc herniation were established in rats by autologous nucleus pulposus transplantation.After successful modeling,rats in the miR-NC,miR-141-3p inhibitor and miR-141-3p mimics groups were injected intrathecally with 10 μL of 20 μmol/L miR-NC,miR-141-3p inhibitor,miR-141-3p mimics,once a day for 28 days,respectively,while those in the normal and model groups were injected with the same volume of saline at the same location at the same time.Paw withdrawal thermal latency threshold was used to evaluate lower limb pain in rats.The mRNA expression of miR-141-3p in dorsal root ganglion tissue was detected by real-time fluorescence quantitative PCR,the levels of inflammatory factors in dorsal root ganglion tissue were detected by ELISA,and the expression of insulin-like growth factor 1/platelet-derived growth factor in dorsal root ganglion tissue was detected by western blot.The correlation between miR-141-3p and insulin-like growth factor 1/platelet-derived growth factor was analyzed. RESULTS AND CONCLUSION:There were no significant differences in all indexes between the miR-NC group and the model group.Paw withdrawal thermal latency threshold was significantly lower in the model group than in the normal group(P＜0.05),significantly lower in the miR-141-3p inhibitor group than the miR-NC group(P＜0.05),and significantly higher in the miR-141-3p mimics group than in the miR-141-3p inhibitor group(P＜0.05).The mRNA expression of miR-141-3p in dorsal root ganglion tissue was significantly lower in the model group than in the normal group(P＜0.05),significantly lower in the miR-141-3p inhibitor group than in the miR-NC group(P＜0.05),and significantly higher in the miR-141-3p mimics group than in the miR-141-3p inhibitor group(P＜0.05).The levels of tumor necrosis factor α,interleukin 1β,and interleukin 1 in dorsal root ganglion tissue were significantly higher in the model group than in the normal group(P＜0.05),significantly higher in the miR-141-3p inhibitor group than in the miR-NC group(P＜0.05),and significantly lower in the miR-141-3p mimics group than in the miR-141-3p inhibitor group(P＜0.05).The protein expressions of insulin-like growth factor 1 and platelet-derived growth factor in dorsal root ganglion tissue were significantly lower in the model group than in the normal group(P＜0.05),significantly lower in the miR-141-3p inhibitor group than in the miR-NC group(P＜0.05),and significantly higher in the miR-141-3p mimics group than in the miR-141-3p inhibitor group(P＜0.05).The expressions of insulin-like growth factor 1 and platelet-derived growth factor showed a positive correlation with miR-141-3p(r=0.904,P＜0.001;r=0.879,P＜0.001).To conclude,miR-141-3p can significantly improve lower limb pain and inhibit inflammation in dorsal root ganglia in rats with lumbar disc herniation,and its mechanism may be related to the promotion of insulin-like growth factor 1/platelet-derived growth factor expression.
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Objective @#To investigate the effect of miR-141-3p on LPS induced A549 cell injury by targeting high mobility group protein 1 (HMGB1) ．@*Methods @#A549 cells derived from type Ⅱ alveolar epithelial cells were taken as the study object，miR-141-3p mimics，mimics NC，HMGB1 gene overexpression plasmid (pcDNA3. 1-HMGB1) and empty Vector were transfected into A549 cells respectively or co-transfected，then 10 μg / ml LPS was used for 24 h．Cell proliferation activity was detected by cell counting kit-8 ( CCK-8) ．The activity of lactate dehydrogenase ( LDH) in the supernatant of cell culture was detected by colorimetry．The apoptosis level of each group was detec- ted by flow cytometry．The levels of interleukin (IL) -1 β , IL-6 and tumor necrosis factor α (TNF-α) were detected by enzyme-linked immunosorbent assay (Elisa) ．Dual luciferase reporter gene assay verified the targeted regulatory relationship between miR-141-3p and HMGB1 . @*Results @#After treatment with LPS ，the proliferative activity of A549 cells and the expression level of miR-141-3p decreased ( P ＜0. 05 ) ，the apoptosis rate increased ( P < 0. 05) ，the levels of IL-1 β , IL-6，TNF-α and the activity of LDH in supernatant increased (P＜0. 05) ．Overex- pression of miR-141-3p increased the proliferation activity of A549 cells treated with LPS (P ＜0. 05 ) ，and de- creased the apoptosis rate and the levels of IL-1 β , IL-6，TNF-α in cells and LDH activity in supernatant (P < 0. 05) ．However，overexpression of HMGB1 gene could reverse the ameliorative effect of miR-141-3p on LPS-in- duced A549 cell injury．Dual luciferase reporter gene experiment confirmed that HMGB1 was the downstream target gene of miR-141-3p．@*Conclusion @# miR-141-3p can inhibit LPS-induced apoptosis，reduce the expression level of inflammatory factors，and improve the damage of A549 cells，which may be related to the targeted regulation of HMGB1 expression.
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Abstract Aim miR-141-5p expression in patients with Early Spontaneous Abortion (ESA) and its correlation with hormone levels during pregnancy were investigated. Methods A total of 70 pregnant women with ESA were selected as the research group, and 70 normal pregnant women who chose abortion for non-medical reasons were selected as the Con group. Serum β-HCG, Progesterone (P), and Estrogen (E2) were detected by enzyme-linked immunosorbent assay. Differentially expressed miRNAs were screened by miRNA microarray analysis. miR-141-5p expression was detected by RT-qPCR, and its correlation with serum β-HCG, P, and E2 levels was analyzed. The diagnostic value of miR-141-5p for ESA was evaluated by the ROC curve. Results Serum β-HCG, P, and E2 were decreased and serum miR-141-5p was increased in patients with ESA. Pearson correlation analysis showed that serum β-HCG, P, and E2 levels were negatively correlated with miR-141-5p expression levels. ROC curve showed that miR-141-5p had a diagnostic value for ESA. Conclusions miR-141-5p is related to hormone levels during pregnancy and is expected to become a new candidate diagnostic marker for ESA.
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AIM: To explore the relationship between the changes of serum circFTO and microRNA-141-3p(miR-141-3p)levels and the different disease stages of diabetes retinopathy.METHODS: A total of 198 patients with type 2 diabetes admitted to our hospital from October 2019 to November 2022 were collected as the study subjects, the patients were grouped into non diabetes retinopathy(NDR)group(70 cases), non proliferative diabetes retinopathy(NPDR)group(66 cases)and proliferative diabetes retinopathy(PDR)group(62 cases)according to different stages; meantime, 67 volunteers with normal physical examination results were collected as the control group. The levels of serum circFTO and miR-141-3p were detected by real-time fluorescent quantitative PCR(qRT-PCR); Pearson correlation analysis was used to examine the correlation between the serum circFTO, miR-141-3p and various indicators in patients with diabetes retinopathy; multivariate Logistic regression analysis was applied to explore the influencing factors of diabetes retinopathy.RESULTS: CircFTO, systolic blood pressure(SBP), and diastolic blood pressure(DBP)in PDR group were higher than those in control group, NDR group and NPDR group, while miR-141-3p and high-density lipoprotein cholesterol(HDL-C)were lower than those in control group, NDR group and NPDR group(P<0.05). Fasting blood glucose(FPG)and glycosylated hemoglobin(HbA1c)in NDR group, NPDR group and PDR group were higher than those in the control group(all P<0.05). The course of disease in PDR group was longer than that in NDR group and NPDR group(P<0.05). Serum circFTO in patients with diabetes retinopathy was positively correlated with SBP, DBP, FPG, HbA1c, and miR-141-3p was negatively correlated with SBP, DBP, FPG, HbA1c(all P<0.05). CircFTO was a risk factor for diabetes retinopathy, and miR-141-3p was a protective factor for diabetes retinopathy(P<0.05).CONCLUSION: Serum circFTO is obviously increased and miR-141-3p is obviously decreased in patients with diabetes retinopathy, both of them are closely related to disease stage, and are expected to become important indicators for evaluating disease progress.
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Objective To investigate the effect and mechanism of miR-141-3p on pulmonary fibrosis in rats with acute respiratory distress syndrome(ARDS).Methods Rats were divided into the control group,the model group,the agomir negative control group and the miR-141-3p agomir group according to random number table,with 10 rats in each group.In addition to the control group,the ARDS rat model was established by lipopolysaccharide(LPS)infusion.Rat alveolar typeⅡepithelial cells RLE-6TN cells were divided into the NC group,the LPS group,the miR-NC group,the miR-141-3p mimics group,the miR-141-3p mimics+pcDNA group and the miR-141-3p mimics+NRF2 and Kelch-like ring associated protein 1(Keap1)group.LPS cell model was established in all groups except the NC group.The mRNA expression levels of miR-141-3p and Keap1 in lung tissue and cells were detected by qPCR.Western blot assay was used to analyze lung tissue and cell epithelial cadherin(E-cadherin),neural cadherin(N-cadherin),microtubule associated protein light chain 3B(LC3B),autophagy associated gene Beclin-1,α-smooth muscle actin(α-SMA),type I collagen(Col-Ⅰ),Keap1 and nuclear factors E2 related factor 2(NRF2)and heme oxygenase 1(HO-1).HE staining and Masson staining were used to observe pathological changes of lung tissue and to estimate the area of lung tissue injury and pulmonary fibrosis.Hydroxyproline(Hyp)in lung tissue was detected by the kit.Levels of inflammatory factor interleukin-1β,tumor necrosis factor(TNF-α)and oxidative stress index malondialdehyde(MDA)and superoxide dismutase(SOD)were detected by ELISA.Dual luciferase reporting experiment was used to verify the targeting relationship between miR-141-3p and Keap1.Results The expression of miR-141-3p was down-regulated and the expression of Keap1 was up-regulated in lung tissue and cells(P＜0.05).Overexpression of miR-141-3p can reduce the degree of pathological damage and fibrosis of lung tissue in rats,Hyp content,and up-regulate expression levels of SOD,E-cadherin,LC3B,Beclin-1,NRF2 and HO-1 in lung tissue and cells,and down-regulate the expression levels of IL-1β,TNF-α,MDA,N-cadherin,α-SMA,Col-I and Keap1(P＜0.05).Overexpression of Keap1 was able to reverse the improvement effect of overexpression of miR-141-3p on alveolar epithelial cell damage in ARDS rats(P＜0.05).Double Luciferase reporter gene experiment confirmed that miR-141-3p and Keap1 may have a targeted regulatory relationship.Conclusion Overexpression of miR-141-3p may activate the Keap1-NRF2/ARE signaling pathway,activate autophagy,inhibit inflammatory response,oxidative stress,and EMT progression,and improve pulmonary fibrosis in ARDS rats.
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Objective:To investigate the effect of miR-141 down-regulation on the damage of renal tubular epithelial cell, and further to explore its mechanism.Methods:The renal tubular epithelial cell line HK-2 cells were divided into normal (5.5 mmol/L D-glucose) group, hypertonic group, high glucose (30 mmol/L D-glucose) group, negative control+high glucose group (transfected with NC inhibitor vector) and si-miR-141+high glucose group (transfected with miR-141 inhibitor vector) . Real time quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression of miR-141. The production of reactive oxygen species (ROS) , cell viability and apoptosis were detected by DCFH-DA fluorescence staining, CCK-8 method and flow cytometry. The expression of Sirt1/Nrf2 signaling pathway related proteins was detected by Western blot. Luciferase reporter gene assay verified the targeting relationship between miR-141 and Sirt1 mRNA.Results:①Compared with the normal group, after transfection with si-miR-141, the relative expression of miR-141 decreased (1.00±0.03 vs 0.52±0.06) , the difference was statistically significant ( F=278.104, P<0.05) ; ② Compared with the normal group [DCFH-DA fluorescence intensity (7.18±0.59) %], the high glucose group [DCFH-DA fluorescence intensity (84.95±3.21) %] cell ROS level was significantly increased, and compared with the high glucose group [DCFH-DA fluorescence intensity (84.95±3.21) %] Compared with the si-miR-141+ high glucose group [DCFH-DA fluorescence intensity (45.10±4.29) %] cell ROS levels were significantly reduced, the difference was statistically significant (all P<0.05) ; ③compared with the normal group (5.13%±0.78) % Compared with the hypertonic group (5.96±0.81) %, the high glucose group (32.76±2.95) % cell apoptosis rate was significantly increased, while the si-miR-141+ high glucose group (17.54%± 2.79) % apoptosis rate was significantly lower in the higher glucose group and the negative control+ high glucose group (33.40%±3.14) %, the difference was statistically significant ( F=221.419, P<0.05) ; ④compared with the normal group (100±3.98) % Compared with the hypertonic group (95.68±5.14) %, the high glucose group (67.24±5.18) % HK-2 cell survival rate was significantly reduced; at the same time, compared with the high glucose group (67.24±5.18) % and Compared with the negative control+ high glucose group (65.33±3.10) %, the si-miR-141+ high glucose group (83.55±5.10) % cell survival rate increased significantly, and the difference was statistically significant ( F=93.008, P<0.05) ; ⑤ Compared with the normal group and the hypertonic group, the expression of Cleaved Caspase 3 protein in the high glucose group increased, while the expression of Sirt1, Nrf2 and HO-1 protein was down-regulated; however, compared with the high glucose group, si- In the miR-141+ high glucose group, Cleaved caspase 3 protein expression decreased, while Sirt1, Nrf2 and HO-1 protein expression increased, the difference was statistically significant (all P<0.05) . Conclusions:Down-regulation of miR-141 can ameliorate high glucose-induced renal tubular epithelial cell damage induced oxidative stress by activating Sirt1/Nrf2 signaling pathway.
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@#[Abstract] Objective: To study the effect of microRNA-141(miR-141) expression regulation on cell proliferation, cell cycle, apoptosis, invasion and migration of human prostate cancer cell line DU145 and its mechanism. Methods: MiR-141 mimics (miR-141 up group) and miR-141 inhibitors (miR-141 down group) were transfected into human prostate cancer DU145 cells by using liposome lipofectamine 2000, and the un-transfection group (Control group) and non-sense miRNA sequence transfection group (NC group) were set. The expression of miRNA-141 in DU145 cells in each group before and after transfection was detected by qPCR. MTT assay was used to detect the proliferation viability and sensitivity to cisplatin (DDP) in DU145 cells of each group. Cell cycle and apoptosis rate of DU145 cells under DDP treatment were detected by Flow cytometry; the changes in cell invasion and migration ability were detected by Transwell method. The protein expressions of VEGF and EGFR in DU145 cells of each group were detected by Western blotting. Results: Compared with the Control and NC group, the level of miRNA-141 expression in the miR-141-down group decreased to (0.18±0.08), the cell proliferation viability decreased significantly while its sensitivity to DDP increased significantly, the cell cycle was blocked in the G0+G1 phase, and the apoptosis rate significantly increased to (46.67±5.86)% while cell invasion rate and migration rate significantly decreased to (44.34±8.32)%, (57.73±6.19)%, and the relative expression levels of VEGF and EGFR decreased to (0.47±0.06), (0.36±0.06), (P<0.05 or P<0.01). But in the miR-141-up group, the level of miRNA-141 expression increased to (4.23±0.53), the cell proliferation viability significantly increased while its sensitivity to DDP decreased significantly, and the cell cycle was promoted into S and G2 phase, the apoptosis rate significantly decreased to (18.77±4.24)% while cell invasion and migration rate significantly increased to (89.94±6.34)%, (94.44±5.84)%, and the relative expression levels of VEGF and EGFR were up to (0.89±0.07), (0.73±0.06),(P<0.05 or P<0.01). Conclusion: miR-141 can act as a growth promoting factor in prostate cancer DU145 cells. miR-141 down-regula‐tion can significantly inhibit the proliferation viability, cell cycle, migration and invasion of DU145 cells, and promote cell apoptosis and DDP-sensitivity, and the mechanism of which may be related with inhibition of VEGF and EGFR protein expressions.
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OBJECTIVE：To study the improvement effects of icariside Ⅱ（ICS Ⅱ）on neurological function of focal cerebral ischemia model rats by regulating miR- 141-3p/Notch/nuclear factor erythroid- 2-related factor 2（Nrf2）axis（miR-141-3p/Notch/ Nrf2）. METHODS ：The rats were divided into sham operation group ，model group ，nimodipine group （20 mg/kg）and ICS Ⅱ low-dose，medium-dose and high-dose groups （4，8，16 mg/kg），with 20 rats in each group. Twenty-four hours after establishing focal cerebral ischemia model ，model rats were given re levant medicine or normal saline intragastrically ，twice a day ，for consecutive 3 d. The neurological deficit of rats in each group was scored ；the volume of cerebral infarction was measured by 2，3， 5-triphenyltetrazolium chloride （TTC）staining；water content of cerebral tissue and the permeability of blood-brain barrier were measured；HE staining was performed to observe the pathological change of cerebral tissue of rats ；the expression of miR- 141-3p in cerebral tissue of rats was measured by qRT-PCR ；the protein expression of Notch and Nrf 2 in cerebral tissue of rats were measured by Western blotting assay. RESULTS ：Compared with sham operation group ，the neurological deficit score ，expression of Notch-1 and Nrf 2 in model group were significantly lowered （P＜0.05）；infarction volume ，brain water content ，the permeability of blood-brain barrier and the expression of miR- 141-3p in cerebral tissue were increased significantly （P＜0.05）；the distribution of cortical cells was disordered ，and inflammatory infiltration and necrosis were observed in a large number of nerve cells. Compared with model group ，the neurological deficit score ，the protein expression of Notch- 1 and Nrf 2 in cerebral tissue were significantly increased in ICS Ⅱgroups（P＜0.05）；infarction volume ，brain water content ，the permeability of blood-brain barrier and the expression of miR- 141-3p in cerebral tissue were decreased significantly （P＜0.05）；the arrangement of cortical cells was regular，and the inflammatory infiltration and necrosis of nerve cells were decreased significantly. CONCLUSIONS ：ICS Ⅱ can promote the recovery of neurological function in focal cerebral ischemic model rats ，which may be related to down-regulation of miR-141-3p and activation of Notch/Nrf 2 axis.
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@#Objective: To investigate the regulatory effect of lncRNA MALAT1/miR-141-3p/ZEB1 axis on the invasion, metastasis and epithelial mesenchymal transition (EMT) of gastric cancer (GC) cells. Methods: Thirty-eight pairs of GC tissues (non-necrotic part) and corresponding adjacent tissues (>5 cm away from tumor tissue) removed by general surgery in Wuhan Commercial Hospital from April 2014 to May 2017 were collected. Meanwhile, normal gastric epithelial GES1 cells and GC cell lines (SGC7901, HGC27, BGC823, MKN45 and MKN28) were selected. The expression level of MALAT1 and miR-141-3p in GC tissues and cell lines were detected by qPCR. The effect of MALAT1 knockdown on proliferation, migration and invasion of SGC7901 cells was determined by CCK-8 assay and Transwell assay. WB was performed for measuring the expression level of ZEB1, E-cadherin, N-cadherin and Vimentin. Dual luciferase reporter gene assay was used to validate the relationship among MALAT1, miR-141-3p and ZEB1. CCK-8 assay and Transwell assay were used to detect the effect of MALAT1/miR-141-3p/ZEB1 axis on biological behaviors of SGC7901 cells. Results: MALAT1 was over-expressed in GC tissues and cell lines (P<0.05 or P<0.01). Knockdown of MALAT1 significantly inhibited the proliferation, migration, invasion and EMT of SGC7901 cells (P<0.05 or P<0.01). The results of dual luciferase reporter gene assay showed that MALAT1 directly targeted miR-141-3p, as well as for miR-141-3p and ZEB1. Further experiment indicated that simultaneous over-expression of miR-141-3p and MALAT1 or ZEB1 could restore the biological behaviors of SGC7901 cells, which were inhibited by miR-141-3p. Conclusion: MALAT1 promotes the invasion, metastasis and EMT of GC SGC7901 cells by down-regulating the inhibitory effect of miR-141-3p on ZEB1.
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@#Objective: To explore the effect of miR-141-3p on the proliferation, invasion and apoptosis of ovarian cancer cells via targeting PTEN and regulating PI3K/Akt pathway. Methods: Collecting twenty-eight cases pairs of ovarian cancerovarian cancer patients with tumor tissues and adjacent tissues were collected from patients, who from April 2014 to October 2017 were treated in the Department of Obstetrics and Gynecology. qPCR was applied to detect the expression of miR-141-3p in ovarian cancer tissues and cell lines. The relationship between miR-141-3p and PTEN was verified by dual-luciferase reporter gene assay. After over-expression or knockdown of miR-141 and PTEN genes, the cell viability, invasion and apoptosis of ovarian cancer A2780 cells were examined by CCK-8 assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. Furthermore, the effect of miR-1413p on PTEN-PI3K/Akt signaling pathway was measured by WB. Results: miR-141-3p is was highly expressed in ovarian cancer tissues and cell lines (P<0.05 or P<0.01). The dual luciferase reporter gene assay confirmed that miR-141-3p targets PTEN was a target of miR-141-3p and downregulates its expression level was down-regulated (P<0.01). Compared with the control group, after knockdown of miR-141-3p, the proliferation ofA2780 cells was significantly inhibited after knockdown of miR-141-3p (at 48 h, 0.36±0.04 vs 0.82± 0.06, P<0.05), and the invasive ability of A2780 cells was significantly reduced (number of transmembrane cells: 215.32±16.04 vs 45.14±7.88, P<0.01), while the apoptotic rate was significantly increased ([1.85±0.26]% vs [9.29±0.65]%, P<0.01). Over-expression of PTEN significantly inhibited the expression of p-Akt and cell proliferation and invasion in A2780 cells (all P<0.01), inhibited cell proliferation and invasion (all P<0.01) and significantly promoted apoptosis (all P<0.01). However, simultaneous over-expression of miR141-3p or addition of IGF-1 wile over-expressing PTEN can offset the above effects. Conclusion: miR-141-3p facilitates the proliferation, invasion and decreases apoptosis of A2780 cells. The mechanism may be related to targeted regulation of PTEN and activation of PI3K/Akt pathway.
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Objective: To detect the expression levels of microRNA200 (miR200) family in the plasma of the breast cancer patients and the normal controls, and to evaluate their potential values in the screening, progression and prognosis evaluation of breast cancer. Methods: A total of 82 cases of plasma samples of the patients with breast cancer (breast cancer group) and 30 cases of healthy plasma samples (control group) were collected. The microRNAs (miRNAs) were extracted from the plasma samples, the expression levels of miR200 family (miR200a, miR200b, miR200c, miR141 and miR429) were quantified by using real-time PCR technique. The receiver-operating characteristic (ROC) curve was used to assess the diagnostic value of miRNAs, and the associations between the levels of miRNAs and the clinicopathological characteristics were analyzed. Cox proportional hazard mode was used for survival analysis. Results: Compared with control group, the expression level of miR141 in the plasma of the patients in breast cancer group was decreased (P 0 . 05). Concuson: MiR200b and miR141 are likely to become the molecular biological parameters for the diagnosis of breast cancer.
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@#Objective: To investigate the relationship between miR-141-3p and transforming growth factorβ2 (TGF-β2), and its effects on the malignant biological behaviors of human prostate cancer cell line C4-2B. Methods:After the transfection of miR-141-3p mimic, the mRNAexpression of miR-141-3p and TGF-β2 in C4-2B cells was detected by qRT-PCR. Bioinformatics method validated the relationship between miR-141-3p and TGF-β2. miR-141-3p mimic alone or with TGF-β2 over-expression vector was transfected into C42B cells, and then Western blotting was used to detect the expression of TGF-β2 protein in C4-2B cells, Hochest33258 staining was used to detect cell apoptosis, and Transwell assay was used to detect the invasion ability of cells in each group. Results:After the transfection of C4-2B cells with miR-141-3p mimic, the level of miR-141-3p increased significantly, and the level of TGF-β2 mRNA decreased significantly (all P<0.01). The activity of luciferase was significantly reduced after the co-transfection with miR-141-3p mimic and wild type report plasmid (P<0.01); However, the activity of luciferase was not obviously changed after co-transfection with miR141-3p mimic and mutant type report plasmid (P>0.05).After co-transfection with miR-141-3p mimic and pc-TGF-β2, the proliferation of C4-2B cells decreased significantly, the number of apoptotic cells increased significantly, and the cell invasion ability decreased significantly (all P<0.01). Conclusion: miR-141-3p inhibits the proliferation and invasion of human prostate cancer C4-2B cells and induces cell apoptosis by targeting TGF-β2.
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Objective To investigate the expression of miR-141 and miR-224 in non-small cell lung cancer (NSCLC) and its clinical significance.Methods The levels of serum miR-141,miR-224 and squamous cell carcinoma associated antigen (SCC-Ag) were detected by RT-PCR in 128 patients with NSCLC,60 patients with benign lesions (benign group) and 60 healthy subjects (control group).To analyze the relationship between the expression levels of miR-141 and miR-224 and the clinicopathological features of NSCLC.The sensitivity and specificity of miR-141,miR-224 and SCC-Ag in the diagnosis of NSCLC were evaluated by ROC curve,and the correlation between serum miR-141 and miR-224,SCC-Ag were analyzed by Pearson correlation analysis in NSCLC patients.Results The levels of serum miR-141,miR-224 and SCC-Ag in NSCLC group were significantly higher than those in the benign group and the control group[miR-141(2-△△Ct):2.56±0.48 vs 1.08±0.24 and 1.02±0.21,miR-224 (2-△△Ct):3.94±0.82 vs 1.42±0.35 and 1.26±0.30,SCC-Ag (ng/ml):2.75±1.36 vs 0.64±0.47 and 0.52±0.24,all P＜0.01].In patients with NSCLC,the levels of serum miR-141 and miR-224 were correlated with pathological stage,pathological grade and lymph node metastasis (P＜0.05).ROC curve analysis showed that the optimal cut-off values of serum miR-141,miR 224 and SCC Ag (ng/ml) for diagnosis of NSCLC were 1.84,2.85 and 2.03,respectively.The AUC (0.913) of the three combined diagnosis of NSCLC was the largest,and the sensitivity and specificity were better,with 92.5 ％ and 82.7 ％,respectively.Pearson correlation analysis showed that serum miR-141 were positively corre lated with miR-224 and SCC-Ag (r=0.782,0.594,all P＜0.01),and serum miR 224 was positively correlated with SCC-Ag (r=0.594,P＜0.01).Conclusion Serum miR-141 and miR-224 are up-regulated in patients with NSCLC and are associated with clinicopathological features,and may be a new biomarker for the diagnosis of NSCLC.
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Objective:This work aims to detect the levels of miR-200c/141 methylation and miR-200c/141 in gastric cancer tissue and investigate the relationship between miR-200c/141 expression and clinical parameters. Methods:The methylation status of miR-200c/141 CpG island and miR-200c/141 in gastric cancer tissue specimens was evaluated by qRT-PCR or BS-MSP method. We analyzed the relationship among the methylation status of miR-200c/141 CpG island, expression level of miR-200c or miR-141, and clinical parame-ters. Results:The status of miR-200c/141 CpG island methylation in gastric cancer tissue was significantly higher compared with that in paracarcinoma tissue. MiR-200c and miR-141 were markedly decreased in gastric cancer tissue compared with those in adjacent tis-sue. MiR-200c/141 CpG island methylation was negatively related with the expression of miR-200c and miR-141 in gastric cancer speci-mens. Conclusion:The upregulation of miR-200c/141 CpG methylation inhibits miR-200c/141 expression in gastric cancer tissue.
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Objective To investigate the role and potential molecular mechanism of the radiosensitivity of esophagus cancer cells.Methods miR-141 mimics or its negative control was transfected into esophagus cancercells KYSE-150,respectively.Radiosensitivity of esophagus cancer cells was determined by CCK-8,flow cytometry and colony formation assay.The expression level of miR-141 was determined by qRT-PCR.Western blot was used to detect the expressions of proliferation-related protein Ki67 and apoptosis-related proteins Bax and Bcl-2.Results After radiation,the expression of miR-141 was decreased in KYSE-150 cells in a dose-dependent manner (t =2.57-8.96,P ＜ 0.05).Upregulation of miR-141 significantly suppressed cell proliferation and colony formation and promoted apoptosis,indicating that overexpression of miR-141 enhanced the radiosensitivity of KYSE-150 cells(t =3.24,P ＜0.05).In addition,the miR-141 mimic significantly reduced the expressions of Ki67 and Bcl-2 protein (t =6.56,8.24,P ＜ 0.01) and inhibited the expression of Bax protein compared with miR-control group (t =3.24,P ＜ 0.01).Conclusions Over-expression of miR-141 enhances the radiosensitivity of esophagus cancer cells by regulating the expressions of proliferation-related protein Ki67 and apoptosisrelated proteins Bax and Bcl-2.
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Objective To assess the effect of miR-141 on proliferation of human oral squamous cell carcinoma and target relationship between miR-141 and EphA2 .Methods pcDNATM6.2-GW-pre-miR-141 was constructed and identified by qRT-PCR.EphA2-WT and EphA2-MT sequences were respectively cloned into pmirGLO plasmid . The potential proliferation function of miR-141 on CAL27 cells was analyzed by MTT .The target relationship be-tween miR-141 and EphA2 was identified by Dual-Luciferase Assay System , qRT-PCR and Western blot .Results We constructed successfully the recombinant plasmids , including pcDNATM6.2-GW-pre-miR-141, pmirGLO-E-phA2-WT and pmirGLO-EphA2-MT, and the transfection efficiency of pre-miR-141 was increased in CAL27 cells compared to control group(P<0.001).miR-141 could suppress the proliferation of CAL27 cells(P<0.05). Furthermore, a significant reduction of luciferase activities of CAL27 cells co-transfected with pre-miR-141 and EphA2-WT(P<0.001).The mRNA(P<0.001) and protein expression levels of EphA2 were decreased in CAL27 cells transfected with pre-miR-141 .Conclusions Overexpression of miR-141 may suppress cell prolifera-tion by targeting at EphA2 in CAL27 cells.
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Objective To determine the expressions of miR-200a, miR-141, miR-205 and miR-34a in epithelial ovarian cancer (EOC) samples and to explore their clinical significance. Methods According to FIGO staging, 44 EOC pa?tients were divided into two groups:early FIGO stage (stageⅠ-Ⅱ, n=15) and late FIGO stage (stageⅢ-Ⅳ, n=29). Expres?sions of 4 miRNAs were detected by real time quantitative PCR, and were compared between two groups. The correlation of 4 miRNAs was calculated. EOC patients were divided into high miRNA expression group and low expression group according to the median value of miRNAs expression. Kaplan-Meier survival analysis and Cox multivariate analysis were used to com?pare the age, FIGO state, tumor residual after operation and post-operative chemotherapy of ovarian cancer between two groups. Results The expression of miR-141 was elevated in stagesⅢandⅣcompared with that of stagesⅠand Ⅱ(P=0.036). There was a positive correlation between expression of miR-141, miR-200a and miR-205, but a negative correlation with miR-34a (P<0.05). There was a positive correlation between miR-200a and miR-205 (P<0.05). Lower miR-200a ex?pression was associated with shorter progress free survival in ovarian cancer analyzed by log-rank test ( P=0.035). The sur?vival rate was significantly higher in FIGO stages ⅠandⅡthan that of FIGO stagesⅢandⅣ(P<0.05). Cox regression analysis revealed that miR-200a, FIGO stage and age were influential factors of overall survival time and progress-free sur?vival time of ovarian cancer, while miR-141, miR-205, miR-34a and tumor residual after operation and post-operative che?motherapy were not influential factors. Conclusion The expression of miR-200a is closely correlated with the progress and prognosis of ovarian cancer and may be used as an independent indicator for ovarian cancer prognosis.
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Objective Our retrospective study is aimed to analyze the correlative clinical features of be-tween expressions of miR -135b and miR-141 in colorectal cancer.Methods Clinical data and specimens of patients with colorectal carcinoma at our hospital from 2013 to 2014 were retrospectively collected .The expres-sions of miR-135 b and miR-141 between colon cancer and matched normal colonic tissues were compared .The correlation between the expressions of miR -135 b and miR-141 in colorectal carcinoma and the clinical charac-teristics were discussed .Results A total of 42 patients was retrospective analyzed .The expressions of miR -135b,miR-141 in the colon cancer tissues were obviously higher than that in the normal colonic tissues .The differences of the expression of miR -141 in the colon cancer tissues of different Dukes stages ,degree of differen-tiation,lymph node metastasis and infiltration depth were all significant .The expressions of miR -135 b and miR-141 displayed a positive linear correlation .Conclusion The expressions of miR-135b,miR-141 in colorec-tal cancer are significantly increased ,and the expressions display a remarkable correlation with the Dukes stages , degree of differentiation ,lymph node metastasis and infiltration depth of tumor .The expressions of miR-135 b and miR-141 demonstrate a positive correlation .
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Background and purpose:MicroRNAs are 19 to 25-nucleotide noncoding RNA molecules. The aim of this article was to investigate the expression and clinical signiifcance of microRNA-141 in childhood B-cell acute lymphoblastic leukemia (ALL). Methods:Bone marrow samples were collected from 35 children with B-cell ALL and 15 children with non hematologic disease. Total RNA was acquired from bone marrow. Real-time PCR was performed to detect the expression level of miR-141. Results:The relative expression level of miR-141 in B-cell ALL group was remarkably lower than those in the control (P<0.05). The expression of miR-141 in newly diagnosed samples was lower than those in Day 30 and Week 12 samples respectively (P<0.05). Besides, the expression of miR-141 in Day 30 samples was lower than those in week 12 samples (P<0.05). The expression of miR-141 in children over 10 years old was signiifcantly lower than those in children under 10 years old (P<0.05). The expression of miR-141 in low-risk group was higher than those in mid-risk and high-risk group respectively (P<0.05), and there was signiifcant difference between mid-risk and high-risk groups (P<0.05). Conclusion:MiR-141 is likely to have tumor suppressor effect and to be a potential prognostic biomarker in childhood B cell ALL.