4.5 Article Retracted Publication

被撤回的出版物: miR-202 functions as a tumor suppressor in non-small cell lung cancer by targeting STAT3 (Retracted article. See vol. 26, 2022)

Journal

MOLECULAR MEDICINE REPORTS
Volume 16, Issue 2, Pages 2281-2289

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2017.6841

Keywords

miR-202; non-small cell lung cancer; signal transducer and activator of transcription 3; tumor suppressor

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MicroRNAs (miRNAs) are a group of non-protein-coding, short single-stranded RNAs, which are considered as promising molecular markers and therapeutic targets in several cancers. The present study explored the expression patterns and functional roles of miR-202 in non-small cell lung cancer (NSCLC). The expression levels of miR-202 were determined in NSCLC tissues and cell lines using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The functional impact of miR-202 overexpression on NSCLC cell viability, migration and invasion were evaluated using Cell Counting Kit-8 reagent and Transwell migration and invasion assays, respectively. The molecular mechanism underlying the tumor suppressive roles of miR-202 on NSCLC was examined using bioinformatics analysis, luciferase reporter assay, RT-qPCR and western blot analysis. In addition, signal transducer and activator of transcription (STAT) 3 was overexpressed to investigate the impact on miR-202-mediated tumor suppression in NSCLC. The results indicated that miR-202 was downregulated in NSCLC tissues and cell lines, and was associated with tumor node metastasis stage and lymph node metastasis. Exogenous miR-202 expression reduced NSCLC cell viability, migration and invasion. Furthermore, STAT3 was identified as a direct target gene of miR-202 in NSCLC. STAT3 overexpression improved miR-202-impaired cell viability, migration and invasion. In conclusion, the present study revealed novel anticancer effects induced by miR-202 upregulation in NSCLC, and indicated that STAT3 may be a molecular target of miR-202.

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