Zheng Fang, Zhang Jiahe, Luo Siyu, Yi Jing, Wang Ping, Zheng Quanqing, Wen Yurong
Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Department of Public Health, Public Health Center, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Oncol Lett. 2016 Oct;12(4):3021-3027. doi: 10.3892/ol.2016.5016. Epub 2016 Aug 16.
Inappropriate expression of microRNA (miR) is strongly associated with carcinogenesis. miR-143 was reported to be one of the most prominent miRs implicated in the genesis and progression of human cancer. However, its correlation with cell proliferation and apoptosis in cervical cancer remains to be fully elucidated. In the present study, it was demonstrated that miR-143 is able to suppress the proliferation of cervical cancer HeLa cells and induce cell apoptosis in a time- and dose-dependent manner. The present study also investigated the potential targets of miR-143, extracellular-signal-regulated kinase 5 (ERK5) and its downstream substrate oncoprotein c-Fos, both of which are involved in cell proliferation and apoptosis. Upon increasing the miR-143 level, the ERK5 and c-Fos protein expression was significantly decreased without the effect of ERK5 transcription. Therefore, miR-143 is able to suppress cell proliferation and induce apoptosis in HeLa cells, potentially through negative regulation of ERK5 at its post-transcriptional stage.
微小RNA(miR)的异常表达与癌症发生密切相关。据报道,miR-143是与人类癌症发生和发展相关的最显著的miR之一。然而,其与宫颈癌细胞增殖和凋亡的相关性仍有待充分阐明。在本研究中,证明了miR-143能够以时间和剂量依赖性方式抑制宫颈癌HeLa细胞的增殖并诱导细胞凋亡。本研究还研究了miR-143的潜在靶标,细胞外信号调节激酶5(ERK5)及其下游底物癌蛋白c-Fos,二者均参与细胞增殖和凋亡。随着miR-143水平的升高,ERK5和c-Fos蛋白表达显著降低,而ERK5转录不受影响。因此,miR-143可能通过在转录后阶段对ERK5的负调控来抑制HeLa细胞的增殖并诱导其凋亡。