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miR-181 通过下调自噬来调节顺铂耐药非小细胞肺癌，其机制是通过 PTEN/PI3K/AKT 通路。

miR-181 regulates cisplatin-resistant non-small cell lung cancer via downregulation of autophagy through the PTEN/PI3K/AKT pathway.

机构信息

Department of Medical Oncology, The People's Hospital of Bozhou, Bozhou, Anhui 236804, P.R. China.

Affiliated Tumor Hospital, Huainan Eastern Hospital Group, Huainan, Anhui 232001, P.R. China.

出版信息

Oncol Rep. 2018 Apr;39(4):1631-1639. doi: 10.3892/or.2018.6268. Epub 2018 Feb 13.

DOI:10.3892/or.2018.6268
PMID:29484437
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5868400/
Abstract

A number of miRNAs have been found to be abnormally expressed or mutated in numerous cancers and thus, are considered to act as oncogenes or tumor suppressor genes. The aim of the present study was to investigate the effect of miR-181 on cisplatin-resistant non-small cell lung cancer (NSCLC). In patients with cisplatin-resistant NSCLC, miR-181 expression was found to be markedly decreased. In addition, in the cisplatin-resistant human lung adenocarcinoma cell line A549/DDP, miR-181 downregulation promoted cell growth and metastasis and inhibited cell apoptosis, whereas miR-181 overexpression exerted the opposite effects. Furthermore, miR-181 downregulation suppressed LC3 and ATG5 protein expression in A549/DDP cells through suppression of the PTEN/PI3K/AKT/mTOR pathway, whereas miR-181 overexpression recovered LC3 and ATG5 protein expression by promoting PTEN/PI3K/AKT/mTOR signaling. In turn, PTEN inhibitors reduced the anticancer effects of miR-181 overexpression on A549/DDP cell growth via the regulation of autophagy through the PI3K/AKT/mTOR pathway. Therefore, miR-181 may be a novel and important regulator of cisplatin-resistant NSCLC by serving a role in the regulation of apoptosis, as an established rate-limiting miRNA target.

摘要

许多 miRNA 在多种癌症中被发现表达异常或突变，因此被认为是癌基因或肿瘤抑制基因。本研究旨在探讨 miR-181 对顺铂耐药非小细胞肺癌（NSCLC）的影响。在顺铂耐药 NSCLC 患者中，发现 miR-181 表达明显下调。此外，在顺铂耐药人肺腺癌细胞系 A549/DDP 中，miR-181 下调促进细胞生长和转移，抑制细胞凋亡，而 miR-181 过表达则产生相反的效果。此外，miR-181 下调通过抑制 PTEN/PI3K/AKT/mTOR 通路抑制 A549/DDP 细胞中的 LC3 和 ATG5 蛋白表达，而 miR-181 过表达通过促进 PTEN/PI3K/AKT/mTOR 信号恢复 LC3 和 ATG5 蛋白表达。反过来，PTEN 抑制剂通过 PI3K/AKT/mTOR 通路调节自噬，降低 miR-181 过表达对 A549/DDP 细胞生长的抗癌作用。因此，miR-181 可能通过作为凋亡调控的一个已确立的限速 miRNA 靶点，成为顺铂耐药 NSCLC 的一种新型重要调控因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08b0/5868400/f4ed7d6fc34b/OR-39-04-1631-g12.jpg
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