目的：探讨miRNA-34c在人脑胶质瘤组织中的表达情况及临床意义。方法应用定量PCR方法对18例WHO分级Ⅱ～Ⅳ级的甲醛固定石蜡包埋的脑胶质瘤标本和外伤或脑出血患者内减压手术获得的5例脑组织标本分别进行miR-34c-3p和miR-34c-5p含量的检...目的：探讨miRNA-34c在人脑胶质瘤组织中的表达情况及临床意义。方法应用定量PCR方法对18例WHO分级Ⅱ～Ⅳ级的甲醛固定石蜡包埋的脑胶质瘤标本和外伤或脑出血患者内减压手术获得的5例脑组织标本分别进行miR-34c-3p和miR-34c-5p含量的检测，比较不同级别胶质瘤和正常脑组织中miR-34c-3p和miR-34c-5p的表达差异，分析miR-34c-3p和miR-34c-5p的表达和胶质瘤恶性程度的相关性。结果与正常脑组织相比，胶质瘤中miR-34c-3p和miR-34c-5p的表达皆显著减少（ P ＜0＊．05），而且miR-34c-3p和miR-34c-5p的表达随着胶质瘤级别或恶性程度的增加分别减少，呈显著的负相关（ miR-34c-3p的spearman相关系数＝－0．856， P ＜0．01；miR-34c-5p的spearman相关系数＝－0．767， P ＜0．01）。结论 MiR-34c在人脑胶质瘤细胞中的表达显著降低，而且表达随着肿瘤分级或恶性程度的增高而减少，与胶质瘤级别的升高呈显著的负相关。 MiR-34c在胶质瘤的进展中有重要的意义，可作为脑胶质瘤临床分级的重要指标。展开更多
Granulosa cells（GCs） are somatic cells of ovary, the behaviors of GCs are important for ovarian function. MicroRNAs（miRNAs） are a class of endogenous 18–24 nucleotide（nt） non-coding RNAs, some of which have bee...Granulosa cells（GCs） are somatic cells of ovary, the behaviors of GCs are important for ovarian function. MicroRNAs（miRNAs） are a class of endogenous 18–24 nucleotide（nt） non-coding RNAs, some of which have been shown to be important regulators of GCs function. miR-34c involved in the regulation of various biological processes and was identified to be a pro-apoptotic and anti-proliferative factor in many cell types. However, the roles of miR-34c in GCs function remain unknown. In this study, we used Annexin V-FITC and Ed U assays to demonstrate that miR-34c exerted pro-apoptotic and anti-proliferative effects in porcine GCs. Dual-luciferase reporter assays, quantitative real-time PCR（q RT-PCR） and Western blotting identified Forkhead box O3a（Fox O3a） as a direct target gene of miR-34c. The overexpression of FoxO3a rescued the phenotypic change caused by miR-34c in porcine GCs. In conclusion, miR-34c regulate the function of porcine GCs by targeting FoxO3a.展开更多
BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the ...BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the effect of miR-34c and its upstream transcription factor E2F1 on paclitaxel combined with cisplatin resistance in GC cells.METHODS Paired GC tissues and adjacent normal tissues were randomly sampled from 74 GC patients.miR-34c and E2F1 were detected by real-time quantitative PCR(qPCR)and Western blot.In addition,the drug resistance of GC cells to paclitaxel and cisplatin was induced by concentration gradient increasing methods,and changes in miR-34c and E2F1 during this process were measured.Furthermore,E2F1 and miR-34c overexpression or underexpression vectors were constructed and transfected into drug-resistant GC cells.MTT was employed to test the sensitivity of cells to paclitaxel combined with cisplatin,qPCR was adopted to detect the expression of miR-34c,Western blot was applied to detect the expression levels of E2F1,drug resistance-related proteins and apoptosis-related proteins,and flow cytometry was used for the determination of cell apoptosis and cell cycle status.RESULTS E2F1 was overexpressed while miR-34c was underexpressed in GC.After inducing GC cells to be resistant to paclitaxel and cisplatin,E2F1 expression increased while miR-34c expression decreased.Both silencing E2F1 and overexpressing miR-34c could increase the sensitivity of drug-resistant GC cells to paclitaxel combined with cisplatin,promote cell apoptosis and inhibit cell proliferation.Among which,silencing E2F1 could reduce the expression of drug resistance-related proteins and apoptosis-related proteins,while over-expression of miR-34c could upregulate the expression of apoptosis-related proteins without affecting the expression of MDR-1,MRP and other drug resistance-related proteins.Rescue experiments demonstrated that inhibiting miR-34c could significantly weaken the sensitization of drug resistant cells,and Si E2F1 to paclitaxel combined with cisplatin.CONCLUSION E2F1 inhibits miR-34c to promote the proliferation of GC cells and enhance the resistance to paclitaxel combined with cisplatin,and silencing E2F1 is conducive to improving the efficacy of paclitaxel combined with cisplatin in GC cells.展开更多
文摘目的：探讨miRNA-34c在人脑胶质瘤组织中的表达情况及临床意义。方法应用定量PCR方法对18例WHO分级Ⅱ～Ⅳ级的甲醛固定石蜡包埋的脑胶质瘤标本和外伤或脑出血患者内减压手术获得的5例脑组织标本分别进行miR-34c-3p和miR-34c-5p含量的检测，比较不同级别胶质瘤和正常脑组织中miR-34c-3p和miR-34c-5p的表达差异，分析miR-34c-3p和miR-34c-5p的表达和胶质瘤恶性程度的相关性。结果与正常脑组织相比，胶质瘤中miR-34c-3p和miR-34c-5p的表达皆显著减少（ P ＜0＊．05），而且miR-34c-3p和miR-34c-5p的表达随着胶质瘤级别或恶性程度的增加分别减少，呈显著的负相关（ miR-34c-3p的spearman相关系数＝－0．856， P ＜0．01；miR-34c-5p的spearman相关系数＝－0．767， P ＜0．01）。结论 MiR-34c在人脑胶质瘤细胞中的表达显著降低，而且表达随着肿瘤分级或恶性程度的增高而减少，与胶质瘤级别的升高呈显著的负相关。 MiR-34c在胶质瘤的进展中有重要的意义，可作为脑胶质瘤临床分级的重要指标。
基金supported by the National Natural Science Foundation of China (31201771)the earmarked fund for the China Agriculture Research System (CARS-36)
文摘Granulosa cells（GCs） are somatic cells of ovary, the behaviors of GCs are important for ovarian function. MicroRNAs（miRNAs） are a class of endogenous 18–24 nucleotide（nt） non-coding RNAs, some of which have been shown to be important regulators of GCs function. miR-34c involved in the regulation of various biological processes and was identified to be a pro-apoptotic and anti-proliferative factor in many cell types. However, the roles of miR-34c in GCs function remain unknown. In this study, we used Annexin V-FITC and Ed U assays to demonstrate that miR-34c exerted pro-apoptotic and anti-proliferative effects in porcine GCs. Dual-luciferase reporter assays, quantitative real-time PCR（q RT-PCR） and Western blotting identified Forkhead box O3a（Fox O3a） as a direct target gene of miR-34c. The overexpression of FoxO3a rescued the phenotypic change caused by miR-34c in porcine GCs. In conclusion, miR-34c regulate the function of porcine GCs by targeting FoxO3a.
文摘BACKGROUND MicroRNA 34c(miR-34c)has been reported to be associated with malignant types of cancer,however,it remains unknown whether miR-34c is involved in chemoresistance in gastric cancer(GC).AIM To investigate the effect of miR-34c and its upstream transcription factor E2F1 on paclitaxel combined with cisplatin resistance in GC cells.METHODS Paired GC tissues and adjacent normal tissues were randomly sampled from 74 GC patients.miR-34c and E2F1 were detected by real-time quantitative PCR(qPCR)and Western blot.In addition,the drug resistance of GC cells to paclitaxel and cisplatin was induced by concentration gradient increasing methods,and changes in miR-34c and E2F1 during this process were measured.Furthermore,E2F1 and miR-34c overexpression or underexpression vectors were constructed and transfected into drug-resistant GC cells.MTT was employed to test the sensitivity of cells to paclitaxel combined with cisplatin,qPCR was adopted to detect the expression of miR-34c,Western blot was applied to detect the expression levels of E2F1,drug resistance-related proteins and apoptosis-related proteins,and flow cytometry was used for the determination of cell apoptosis and cell cycle status.RESULTS E2F1 was overexpressed while miR-34c was underexpressed in GC.After inducing GC cells to be resistant to paclitaxel and cisplatin,E2F1 expression increased while miR-34c expression decreased.Both silencing E2F1 and overexpressing miR-34c could increase the sensitivity of drug-resistant GC cells to paclitaxel combined with cisplatin,promote cell apoptosis and inhibit cell proliferation.Among which,silencing E2F1 could reduce the expression of drug resistance-related proteins and apoptosis-related proteins,while over-expression of miR-34c could upregulate the expression of apoptosis-related proteins without affecting the expression of MDR-1,MRP and other drug resistance-related proteins.Rescue experiments demonstrated that inhibiting miR-34c could significantly weaken the sensitization of drug resistant cells,and Si E2F1 to paclitaxel combined with cisplatin.CONCLUSION E2F1 inhibits miR-34c to promote the proliferation of GC cells and enhance the resistance to paclitaxel combined with cisplatin,and silencing E2F1 is conducive to improving the efficacy of paclitaxel combined with cisplatin in GC cells.
