Expression of miR-133b in prostate cancer and its effect on the proliferation of tumor cells
10.13602/j.cnki.jcls.2017.05.08
- VernacularTitle:miR-133b在前列腺癌中的表达及其对肿瘤细胞增殖的影响
- Author:
Lu PENG
;
Cong LIN
- Keywords:
prostate cancer;
microRNA-133b;
positive regulatory domain I-binding factor 16;
proliferation
- From:
Chinese Journal of Clinical Laboratory Science
2017;35(5):349-352
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression level of miR-133b in cancer tissues of patients with prostate cancer and its effect on the proliferation of prostate cancer cells.Methods The total RNAs in resected prostate cancer tissues and adjacent tissues from 30 patients with prostate cancer were extracted and reversely transcripted into cDNA,and then the expression levels of miR-133b were detected by real-time quantitative PCR.The correlations between the expression levels of miR-133b and the patients' clinicopathological features were analyzed.The expression of positive regulatory domain I-binding factor 16 (PRDM16) and proliferation of PC-3 cells transfected with miR-133b mimics by LipofectamineTM 3000 were determined by real-time quantitative PCR and the CCK8 method,respectively.Results The expression levels of miR-133b in prostate cancer tissues [(16.85 ± 0.94) × 10-4] was significantly lower than that in adjacent tissues [(22.95 ± 1.567) × 10-4,t =3.335,P ＜ 0.01].The expression levels of PRDM16 in PC-3 cells transfected with miR-133b mimics were significantly lower than that in the control group (0.371 ±0.031 vs 1.000 ±0.022,t =12.53,P ＜ 0.01).The proliferation ability of PC3 cells transfected with miR-133b mimics for 72 hours was significantly lower than that in the control group (t =6.811,P ＜ 0.01).Similarly,the proliferation ability of PC-3 cells transfected with PRDM16 inhibitor for 72 hours was also significantly lower than that in the control group (t =9.048,P ＜0.01).Conclusion The expression levels of miR-133b in prostate cancer tissues are significantly down-regulated,which regulate the proliferation of prostate cancer cells possibly through PRDM16.
