Research Papers:

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

Huaqi Wang, Li Wang, Guojun Zhang _, Chunya Lu, Heying Chu, Rui Yang and Guoqiang Zhao

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Oncotarget. 2018; 9:7501-7512. https://doi.org/10.18632/oncotarget.23483

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Huaqi Wang1, Li Wang2, Guojun Zhang1, Chunya Lu1, Heying Chu1, Rui Yang1 and Guoqiang Zhao2

1Department of Respiratory Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China

2School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, P.R. China

Correspondence to:

Guojun Zhang, email: [email protected]

Guoqiang Zhao, email: [email protected]

Keywords: MALAT1; cisplatin; resistance; miR-101-3p; myeloid cell leukemia 1

Received: September 27, 2017     Accepted: November 14, 2017     Published: December 14, 2017


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.

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