J Cancer 2022; 13(7):2040-2049. doi:10.7150/jca.65167 This issue

Research Paper

miR-1247-3p targets STAT5A to inhibit lung adenocarcinoma cell migration and chemotherapy resistance

Jiansheng Lin1, Xinyang Zheng1, Xikun Tian2, Jun Guan1✉, Haizhan Shi1✉

1. Department of cardiothoracic surgery, The First Hospital of Putian City, No 449 Nanmen West Road, 351100, Chengxiang District, Putian City, Fujian Province, China.
2. Chosenmed technology (Beijing) Co., Ltd, No. 156, Jinghai 4th Road, Tongzhou District, Beijing, China.

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Citation:
Lin J, Zheng X, Tian X, Guan J, Shi H. miR-1247-3p targets STAT5A to inhibit lung adenocarcinoma cell migration and chemotherapy resistance. J Cancer 2022; 13(7):2040-2049. doi:10.7150/jca.65167. Available from https://www.jcancer.org/v13p2040.htm

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Abstract

Graphic abstract

Background: Although several advancements have been achieved in research and treatment of lung adenocarcinoma in the past few years, the mechanism concerning cancerous cell migration and the cause of chemoresistance remains ambiguous. This research aimed to explore the impact of miR-1247-3p in lung adenocarcinoma.

Methods: The mRNA expression of miR-1247-3p and STAT5A were conducted with qRT-PCR. Lentiviral vectors containing miR-1247-3p mimics and inhibitors were constructed. Cell migration were examined using Transwell assay. To observe chemotherapy resistance, Docetaxel, Doxorubicin, and Gefitinib were used. DIANA, miRDB, and TargetScan databases were applied to detect target genes. The binding sites were verified by double luciferase assay.

Results: Low expression of miR-1247-3p was observed in lung adenocarcinoma tissues and cell lines. Its expression was lower in advanced stages. Cell migration of lung adenocarcinoma was inhibited by miR-1247-3p, and it could negatively regulate the process of chemoresistance. miR-1247-3p directly binds to 3' UTR of STAT5A mRNA, and it functions via targeting STAT5A.

Conclusions: miR-1247-3p acted as a potential governor monitoring cell migration and chemotherapy resistance of LUAD by interacting with STAT5A. It has the potential to be exploited as novel therapeutic target for LUAD in the future.

Keywords: miR-1247-3p, lung adenocarcinoma, STAT5A, cell migration, chemoresistance