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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.

SUBMITTER: Wang H 

PROVIDER: S-EPMC5800919 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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

Wang Huaqi H   Wang Li L   Zhang Guojun G   Lu Chunya C   Chu Heying H   Yang Rui R   Zhao Guoqiang G  

Oncotarget 20171214 7


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 show  ...[more]

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