MiR-15a and miR-16 induce autophagy and enhance chemosensitivity of Camptothecin.
MiR-15a and miR-16 induce autophagy and enhance chemosensitivity of Camptothecin.
复制标题
miR-15a 和 miR-16 诱导自噬并增强喜树碱的化疗敏感性
DOI：
10.1080/15384047.2015.1040963
复制
发表时间：
2015
影响因子：
3.6
通讯作者：
Zhang Y
中科院分区：
文献类型：
--
作者：
Huang N;Wu J;Qiu W;Lyu Q;He J;Xie W;Xu N;Zhang Y
据报道，持续或过度的自噬促进化疗期间癌细胞死亡，通过增强诱导凋亡或介导自噬细胞死亡。在这里，我们表明miR-15 a和miR-16是自噬的有效诱导剂。Rictor是mTORC 2复合物的一个组成部分，被miR-15 a/16直接靶向。miR-15 a/16过表达或内源性Rictor缺失可减弱mTORC 1和p70 S6 K的磷酸化，抑制人宫颈癌HeLa细胞的增殖和G1/S细胞周期转换。此外，miR-15 a/16显著增强抗癌药物喜树碱（CPT）诱导的HeLa细胞自噬和凋亡性细胞死亡。总的来说，这些数据表明miR-15 a/16诱导的自噬部分地有助于其抑制细胞增殖和增强CPT的化疗功效。
It has been reported that persistent or excessive autophagy promotes cancer cell death during chemotherapy, either by enhancing the induction of apoptosis or mediating autophagic cell death. Here, we show that miR-15a and miR-16 are potent inducers of autophagy. Rictor, a component of mTORC2 complex, is directly targeted by miR-15a/16. Overexpression of miR-15a/16 or depletion of endogenous Rictor attenuates the phosphorylation of mTORC1 and p70S6K, inhibits cell proliferation and G1/S cell cycle transition in human cervical carcinoma HeLa cells. Moreover, miR-15a/16 dramatically enhances anticancer drug camptothecin (CPT)-induced autophagy and apoptotic cell death in HeLa cells. Collectively, these data demonstrate that miR-15a/16 induced autophagy contribute partly to their inhibition of cell proliferation and enhanced chemotherapeutic efficacy of CPT.