miR-133b在前列腺癌中的表达及其对肿瘤细胞增殖的影响

Expression of miR-133b in prostate cancer and its effect on the proliferation of tumor cells

目的检测miR-133b在前列腺癌患者癌组织中的表达水平及其对前列腺癌细胞增殖的影响。方法提取30例手术切除的前列腺组织癌和配对癌旁组织中的总RNA,并逆转录为c DNA,实时荧光定量PCR检测癌组织及癌旁组织中miR-133b的表达水平,并分析其与患者临床病理参数之间的相关性;用脂质载体将miR-133b模拟物转染入PC-3细胞中,检测PR结构域结合因子16(PRDM16)表达情况;CCK8实验检测转染miR-133b模拟物后PC-3细胞增殖变化情况。结果前列腺癌组织中miR-133b的表达水平(16.85±0.939)×10^(-4)低于癌旁组织(22.95±1.567)×10^(-4),差异有统计学意义(t=3.335,P<0.01)。PC-3细胞转染miR-133b模拟物后,模拟物转染组中PRDM16表达水平较对照组明显降低,差异有统计学意义(0.371±0.031vs 1.000±0.022,t=12.53,P<0.01);转染miR-133b模拟物72 h后,模拟物转染组的PC-3细胞增殖能力低于阴性对照组,差异有统计学意义(t=6.811,P<0.01);而PRDM16抑制剂转染PC-3细胞72 h后的细胞增殖能力也低于阴性对照组(t=9.048,P<0.01)。结论 miR-133b在前列腺癌组织中的表达下调,其可能通过PRDM16控制前列腺肿瘤细胞增殖。

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 de- tected 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, re- spectively. Results The expression levels of miR-133b in prostate cancer tissues [ （ 16.85 ± 0.94 ） x 10 -4 ] was significantly lower than that in adjacent tissues [ （22.95 ± 1. 567） x 10 -4, t =3,335, P 〈 0.01 ]. The expression levels of PRDM16 in PC-3 cells trans- feeted 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 〈 O. O1 ）. The proliferation ability of PC3 cells transfected with miR-133b mimics for 72 hours was significantly lower than that in the con- trol group （ t = 6.811, P 〈 O. 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. O1 ）. Conclusion The expression levels of miR-133b in pros- tate cancer tissues are significantly down-re±ulated, which regulate the oroliferation of orostate cancer cells possibly through PRDM16.