Tianjin Life Science Research Center and Basic Medical School, Tianjin Medical University, Tianjin 300070, China.
FEBS Lett. 2013 Mar 1;587(5):488-95. doi: 10.1016/j.febslet.2013.01.016. Epub 2013 Jan 18.
MiR-214 has been shown to inhibit cell growth, migration and invasion. Here we demonstrate that ectopic expression of miR-214 reduces cell survival, induces apoptosis and enhances sensitivity to cisplatin through directly inhibiting Bcl2l2 expression in cervical cancer HeLa and C-33A cells. Further analysis reveals that apoptosis induced by miR-214 is correlated with increased expression of Bax, caspase-9, caspase-8 and caspase-3. Moreover, we show that miR-214 is regulated by DNA methylation and histone deacetylation. Taken together, these data suggest that miR-214 might be a candidate target for the development of novel therapeutic strategies to treat cervical cancer.
miR-214 已被证明能够抑制细胞生长、迁移和侵袭。在这里，我们证明，miR-214 的异位表达通过直接抑制宫颈癌 HeLa 和 C-33A 细胞中 Bcl2l2 的表达，降低细胞存活率，诱导细胞凋亡，并增强顺铂的敏感性。进一步的分析表明，miR-214 诱导的细胞凋亡与 Bax、caspase-9、caspase-8 和 caspase-3 的表达增加有关。此外，我们还表明，miR-214 受 DNA 甲基化和组蛋白去乙酰化的调控。综上所述，这些数据表明，miR-214 可能是开发治疗宫颈癌的新型治疗策略的候选靶点。
