Open AccessmiR‑497 inhibits the proliferation and migration of A549 non‑small‑cell lung cancer cells by targeting FGFR1
Author(s) -
Qibin Huang,
Hongtao Li,
Xiaofeng Dai,
Di Zhao,
Bingfeng Guan,
Xin Wen
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10611
Subject(s) - fibroblast growth factor receptor 1 , transfection , cancer research , cell growth , oncogene , microrna , biology , protein kinase b , a549 cell , cell cycle , signal transduction , lung cancer , cancer , cell , microbiology and biotechnology , fibroblast growth factor , cell culture , medicine , receptor , gene , biochemistry , genetics
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.