MicroRNA-30c-5p ameliorates hypoxia-reoxygenation-induced tubular epithelial cell injury via HIF1α stabilization by targeting SOCS3

作者：Yanfang Zou, Weitang Liao, Zongjie Fu, Qian Zhao, Yongxi Chen, Wen Zhang · 发表于：Oncotarget · 年份：2017 · DOI：10.18632/oncotarget.21582 · 被引用次数：17 · 研究领域：Cancer, Hypoxia, and Metabolism、MicroRNA in disease regulation、Nanoplatforms for cancer theranostics

// Yan-Fang Zou 1 , Wei-Tang Liao 1 , Zong-Jie Fu 1 , Qian Zhao 2 , Yong-Xi Chen 1 and Wen Zhang 1 1 Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, PR China 2 Cellular Differentiation and Apoptosis Laboratory, Key Laboratory of National Ministry of Education, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, PR China Correspondence to: Wen Zhang, email: zhangwen255@163.com Keywords: hypoxia-reoxygenation, microRNA, apoptosis, hypoxia-inducible factor-1α Received: July 10, 2017      Accepted: September 03, 2017      Published: October 06, 2017 ABSTRACT The cellular hypoxia-reoxygenation (H/R) model is an ideal method to study ischemia-reperfusion injury, which is associated with high mortality. The role of microRNA-30c-5p (miR-30c-5p) in the H/R epithelial cell model remains unknown. In the current study, we observed a significant reduction in apoptosis when miR-30c-5p was up-regulated. We also found decreased levels of C-caspase-3 (C-CASP3) and Bcl-2-associated X (BAX) proteins and increased levels of B-cell lymphoma-2 (BCL2). Epidermal growth factor receptor (EGFR) showed similar results. Down-regulating miR-30c-5p increased the levels of apoptosis and C-CASP3 and BAX expression; additionally, cell proliferation was inhibited. Hypoxia-inducible factor 1α (HIF1α) protein expression levels were up-regulated in response to up-regu...