Zhang Yan, Meng Xia, Li Cheng, Tan Zhoulin, Guo Xinwei, Zhang Zhiting, Xi Tao
School of Life Science and Technology, China Pharmaceutical University, Nanjing, 210009, People's Republic of China.
Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, Nanjing, 210009, People's Republic of China.
Biotechnol Lett. 2017 Jul;39(7):959-966. doi: 10.1007/s10529-017-2325-2. Epub 2017 Mar 23.
To demonstrate that miR-9 inhibits autophagy by down-regulating Beclin1 and thus enhances the sensitivity of A549 cells to cisplatin.
MiR-9 inhibited Beclin1 expression by binding to its 3'UTR. The inhibition decreased the cisplatin-induced autophagy in A549 cells, evidenced by the decreased expression of LC3II and GFP-LC3 puncta and the increased expression of P62. Upregulation of miR-9 level enhanced the sensibility of A549 cells to cisplatin and increased the cisplatin-induced apoptosis. Overexpression of Beclin1 reversed above effects of miR-9 mimics, cisplatin-induced autophagy was increased and apoptosis was decreased.
MiR-9 inhibits autophagy via targeting Beclin1 3'UTR and thus enhances cisplatin sensitivity in A549 cells.
证明miR-9通过下调Beclin1抑制自噬，从而增强A549细胞对顺铂的敏感性。
miR-9通过与Beclin1的3'UTR结合抑制其表达。这种抑制降低了顺铂诱导的A549细胞自噬，表现为LC3II和GFP-LC3斑点表达降低以及P62表达增加。miR-9水平上调增强了A549细胞对顺铂的敏感性，并增加了顺铂诱导的细胞凋亡。Beclin1的过表达逆转了miR-9模拟物的上述作用，顺铂诱导的自噬增加而细胞凋亡减少。
miR-9通过靶向Beclin1的3'UTR抑制自噬，从而增强A549细胞对顺铂的敏感性。
