miR-202 functions as a tumor suppressor in non-small cell lung cancer by targeting STAT3
Autor: | Nana Zhao, Zhonghai Zhao, Bin Lv, Li Zhang, Yan Lv |
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Rok vydání: | 2017 |
Předmět: |
Male
STAT3 Transcription Factor 0301 basic medicine Cancer Research Lung Neoplasms Cell Survival Cell Down-Regulation Biology medicine.disease_cause Biochemistry 03 medical and health sciences 0302 clinical medicine Cell Movement Carcinoma Non-Small-Cell Lung Cell Line Tumor microRNA Genetics medicine Humans Viability assay 3' Untranslated Regions Molecular Biology Aged Neoplasm Staging Base Sequence Oncogene Antagomirs Cancer Middle Aged Cell cycle medicine.disease Molecular medicine respiratory tract diseases MicroRNAs 030104 developmental biology medicine.anatomical_structure Oncology A549 Cells Lymphatic Metastasis 030220 oncology & carcinogenesis Cancer research Molecular Medicine Female Carcinogenesis Sequence Alignment |
Zdroj: | Molecular Medicine Reports. 16:2281-2289 |
ISSN: | 1791-3004 1791-2997 |
Popis: | 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. |
Databáze: | OpenAIRE |
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