miR‑497 inhibits the proliferation and migration of A549 non‑small‑cell lung cancer cells by targeting FGFR1
Autor: | Qibin Huang, Wen Xia, Bingfeng Guan, Di Zhao, Hongtao Li, Xiaofeng Dai |
---|---|
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Cancer Research Lung Neoplasms Tumor suppressor gene Biochemistry 03 medical and health sciences 0302 clinical medicine Cell Movement Carcinoma Non-Small-Cell Lung microRNA Genetics Humans Receptor Fibroblast Growth Factor Type 1 Molecular Biology Protein kinase B Cell Proliferation Oncogene Cell growth Chemistry Cell cycle Gene Expression Regulation Neoplastic stomatognathic diseases MicroRNAs 030104 developmental biology Oncology A549 Cells 030220 oncology & carcinogenesis Cancer cell Cancer research Molecular Medicine Signal transduction |
Zdroj: | Molecular medicine reports. 20(4) |
ISSN: | 1791-3004 |
Popis: | Fibroblast growth factor receptor 1 (FGFR1) signaling has been reported to contribute to the carcinogenic progression of various cancer types. Previous studies have demonstrated that FGFR1 expression is increased in non‑small cell lung cancer (NSCLC) and promotes cancer cell metastasis. However, the molecular mechanisms underlying increased FGFR1 expression in NSCLC remains largely unknown. In the current study, microRNA (miR)‑497 levels were observed to be inversely correlated with FGFR1 expression in tumor samples from patients with NSCLC. In the NSCLC cell line A549, miR‑497 overexpression inhibited cell proliferation and migration. Increased expression of miR‑497 led to a reduction in FGFR1 expression, at the mRNA and protein levels. In addition, transfection of miR‑497 mimics inactivated the protein kinase B (AKT) and c‑Jun N‑terminal kinase (JNK) signaling pathways, as reduced matrix metallopeptidase 26 expression; all of which are regulated by FGFR1. Using TargetScan software, FGFR1 was also identified as a predicted target gene of miR‑497, and a dual luciferase reporter assay confirmed that miR‑497 directly regulated FGFR1. Transfection of a recombinant FGFR1 overexpression vector reversed miR‑497 mimic‑induced arrest of cell growth and migration in A549 cells. In conclusion, the results of the present study identified miR‑497 as a potential tumor suppressor gene in NSCLC that may function via repressing FGFR1 expression, and AKT and JNK signaling. |
Databáze: | OpenAIRE |
Externí odkaz: |