MALAT1/miR-101-3p/MCL1 axis mediates cisplatin resistance in lung cancer.

Abstract

In this study, we investigated the mechanism by which lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) mediates cisplatin resistance in lung cancer. Lung cancer patients with high MALAT1 levels were associated with cisplatin resistance and low overall survival. Moreover, cisplatin-resistant A549/DDP cells showed higher MALAT1 expression than cisplatin-sensitive lung cancer cells (A549, H460, H1299 and SPC-A1). Dual luciferase reporter and RNA immunoprecipitation assays showed direct binding of miR-101-3p to MALAT1. MALAT1 knockdown in lung cancer cells resulted in miR-101-3p upregulation and increased cisplatin sensitivity. In addition, miR-101-3p decreased myeloid cell leukemia 1 (MCL1) expression by binding to the 3'-untranslated region (3'-UTR) of its mRNA. These results demonstrate that MALAT1/miR-101-3p/MCL1 signaling underlies cisplatin resistance in lung cancer.

• Authors: Huaqi Wang, Li Wang, Guojun Zhang, Chunya Lu, Heying Chu, Rui Yang, Guoqiang Zhao
• Journal: Oncotarget (Oncotarget) Vol. 9 Issue 7 Pg. 7501-7512 (Jan 26 2018) ISSN: 1949-2553 [Electronic] United States
• PMID: 29484127 (Publication Type: Journal Article)