Oncogenic miR-137 contributes to cisplatin resistance via repressing CASP3 in lung adenocarcinoma

NCUIR > college of Health Sciences and Technology > Department of Biomedical Sciences and Engineering > journal & Dissertation > Item 987654321/102862

Please use this identifier to cite or link to this item: https://ir.lib.ncu.edu.tw/handle/987654321/102862

Title:	Oncogenic miR-137 contributes to cisplatin resistance via repressing CASP3 in lung adenocarcinoma
Authors:	許藝瓊;Su, Te-Jen;Ku, Wen-Hui;Chen, Hsuan-Yu;Hsu, Yi-Chiung;Hong, Qi-Sheng;Chang, Gee-Chen;Yu, Sung-Liang;Chen, Jeremy Jw
Contributors:	生醫理工學院生醫科學與工程學系
Keywords:	Original
Date:	2016-01-01
Issue Date:	2026-04-23 11:18:18 (UTC+8)
Publisher:	e-Century Publishing Corporation;United States: e-Century Publishing Corporation
Abstract:	摘要： Although targeted therapy can prolong the survival of non-small cell lung cancer (NSCLC) patients with EGFR mutations, chemotherapy still is the choice for patients with wild-type EGFR or failure in targeted therapy. However, most of the patients will eventually develop chemoresistance. Our previous study showed that miR-137 is a risky microRNA and is associated with poor prognosis in NSCLC patients. Here we investigated the role of miR-137 in cisplatin resistance in lung adenocarcinoma patients. Our data indicated that miR-137 overexpression increases the survival of lung cancer cells exposed to cisplatin and decreases cisplatin-induced apoptosis. Through computational prediction and microarray, we identified caspase-3 (CASP3) as a potential target of miR-137. Luciferase reporter and site-directed mutagenesis assays demonstrated that miR-137 downregulates CASP3 through binding to its 3'-UTR. Moreover, the endogenous CASP3 can be modulated by overexpressing or silencing miR-137 in lung adenocarcinoma cell lines regardless of EGFR status. Suppression of CASP3 by miR-137 provides cancer cells with anti-apoptotic ability, leading to cisplatin resistance. Immunohistochemistry results revealed an inverse correlation between miR-137 and CASP3 expressions in lung adenocarcinoma patients. Together, our data provide a new chemoresistance mechanism in lung adenocarcinoma and a possible target to control chemoresistance in lung adenocarcinoma patients. 其他題名： Am J Cancer Res 出版者： United States: e-Century Publishing Corporation 出版日期： 2016-01-01 出處： American journal of cancer research, 2016-01, Vol.6 (6), p.1317-1330 版權： AJCR Copyright © 2016 2016 識別號： ISSN: 2156-6976 識別號： EISSN: 2156-6976 識別號： PMID: 27429846
Appears in Collections:	[Department of Biomedical Sciences and Engineering ] journal & Dissertation

Files in This Item:

File	Description	Size	Format
index.html		0Kb	HTML	16	View/Open

社群 sharing

Loading...