MiR-30c-5p/ROCK2 axis regulates cell proliferation, apoptosis and EMT via the PI3K/AKT signaling pathway in HG-induced HK-2 cells.
MiR-30c-5p/ROCK2 axis regulates cell proliferation, apoptosis and EMT via the PI3K/AKT signaling pathway in HG-induced HK-2 cells.
复制标题
在高糖诱导的HK - 2细胞中，miR - 30c - 5p/ROCK2轴通过PI3K/AKT信号通路调控细胞增殖、凋亡及上皮 - 间充质转化。
DOI：
10.1515/biol-2020-0089
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发表时间：
2020
影响因子：
2.2
通讯作者：
Cui X
中科院分区：
文献类型：
--
作者：
Cui L;Yu M;Cui X
糖尿病肾病（DN）是糖尿病最常见的并发症之一。越来越多的证据表明microRNA-30c-5p（miR-30c-5p）参与DN的发病机制，但其机制尚未明确。因此，本研究旨在体外研究miR-30c-5p在人类DN进展中的生物学作用。与对照组相比，DN组织和高糖诱导的HK-2细胞的miR-30c-5p水平显着降低，而ROCK2表达显着升高。此外，miR-30c-5p 模拟物明显促进细胞增殖并阻止细胞凋亡和上皮间质转化（EMT）。然而，ROCK2是miR-30c-5p的靶基因，体外上调ROCK2可逆转miR-30c-5p模拟物对细胞增殖、凋亡和EMT的影响。此外，DN的发病机制由miR-30c-5p/ROCK2轴通过PI3K/AKT通路调控。 MiR-30c-5p通过PI3K/AKT通路靶向ROCK2调节细胞增殖、凋亡和EMT，为临床治疗DN提供了新的潜在靶点。
Diabetic nephropathy (DN) is one of the most common complications of diabetes mellitus. Increasing evidence suggests that microRNA-30c-5p (miR-30c-5p) participates in the pathogenesis of DN, but the mechanism has not been clearly understood. Therefore, this study aimed to investigate the biological role of miR-30c-5p in human DN progression in vitro. Compared with the controls, DN tissues and high glucose-induced HK-2 cells had significantly reduced miR-30c-5p levels, while ROCK2 expression was prominently elevated. Additionally, the miR-30c-5p mimic distinctly facilitated cell proliferation and blocked cell apoptosis and epithelial–mesenchymal transition (EMT). However, ROCK2 was a target gene of miR-30c-5p, and the effects of miR-30c-5p mimic on cell proliferation, apoptosis and EMT were reversed by ROCK2 upregulation in vitro. Furthermore, the pathogenesis of DN was regulated by the miR-30c-5p/ROCK2 axis via the PI3K/AKT pathway. MiR-30c-5p regulating cell proliferation, apoptosis and EMT through targeting ROCK2 via the PI3K/AKT pathway provides the novel potential target for clinical treatment of DN.
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影响因子：
64.5
作者：
Manning BD;Toker A
通讯作者：
Toker A
影响因子：
3.7
作者：
Lin G;Brownsey RW;Macleod KM
通讯作者：
Macleod KM
影响因子：
6.6
作者：
Bai, Xiaoyan;Geng, Jian;Liu, Xiaoting
通讯作者：
Liu, Xiaoting
影响因子：
19.6
作者：
Kanda, T;Wakino, S;Saruta, T
通讯作者：
Saruta, T
DOI：
10.1038/nrd4140
发表时间：
2013-11
期刊：
Nature reviews. Drug discovery
影响因子：
--
作者：
Ling H;Fabbri M;Calin GA
通讯作者：
Calin GA