Chang D L, Wei W, Yu Z P, Qin C K
Pharmazie. 2017 Jun 1;72(6):338-343. doi: 10.1691/ph.2017.7406.
Currently, a lot of microRNAs (miRNAs) have been confirmed to be closely related with liver cancer occurrence and development. This study was aimed to explore the role of miR-152-5p in liver cancer. HepG2 and MHCC97 cells were transfected with miR-152-5p mimic, inhibitor or corresponding scramble controls, respectively. The expression level of miR-152-5p in transfected cells was detected by qPCR. Cell viability, apoptosis, migration and invasion of miR-transfected cells were measured to determine the effect of miR-152-5p on the activity of hepatoma cells. The protein expressions of fork head transcription factor O (FOXO) and apoptosis related factors in miR-transfected cells were detected by western blot assay. In addition, western blot was used to detect the relationship of FOXO expression and mainly factors of the JNK signaling pathway after concurrent treatment with miR-152-5p mimic and JNK inhibitor. The results showed that the miR-152-5p was effectively overexpressed or repressed in both HepG2 and MHCC97 cells. Overexpression of miR-152-5p inhibited cell viability, promoted apoptosis, and reduced migration and invasion. In these cells, miR-152-5p overexpression activated the expression of apoptosis-related factors and upregulated the expression of FOXO by activating the phosphorylation of mainly factors in the JNK pathway. miR-152-5p might be a potential anti-tumor factor for liver cancer treatment.
目前,大量微小RNA(miRNA)已被证实与肝癌的发生发展密切相关。本研究旨在探讨miR-152-5p在肝癌中的作用。分别用miR-152-5p模拟物、抑制剂或相应的对照序列转染HepG2和MHCC97细胞。通过qPCR检测转染细胞中miR-152-5p的表达水平。检测miR转染细胞的细胞活力、凋亡、迁移和侵袭情况,以确定miR-152-5p对肝癌细胞活性的影响。通过蛋白质印迹法检测miR转染细胞中叉头转录因子O(FOXO)和凋亡相关因子的蛋白表达。此外,在用miR-152-5p模拟物和JNK抑制剂联合处理后,用蛋白质印迹法检测FOXO表达与JNK信号通路主要因子的关系。结果表明,miR-152-5p在HepG2和MHCC97细胞中均能有效过表达或被抑制。miR-152-5p的过表达抑制细胞活力,促进凋亡,并减少迁移和侵袭。在这些细胞中,miR-152-5p的过表达激活凋亡相关因子的表达,并通过激活JNK途径主要因子的磷酸化上调FOXO的表达。miR-152-5p可能是肝癌治疗的潜在抗肿瘤因子。