RETRACTED: Downregulation of fibroblast growth factor 5 inhibits cell growth and invasion of human nonsmall‐cell lung cancer cells

Abstract

The morbidity and mortality rates of nonsmall‐cell lung cancer (NSCLC) have increased in recent years. We aimed to explore the biological role of fibroblast growth factor 5 (FGF5) in NSCLC. We first established that the expression of FGF5 was increased in NSCLC tissues compared with the normal adjacent tissues. The expression of FGF5 was also increased in NSCLC cell lines. The effect of FGF5 silencing on cell proliferation, cell cycle, apoptosis, migration, and invasion of H661 and CALU1 cells was then examined. Downregulation of FGF5 significantly inhibited cell proliferation and induced G1 phase cell cycle arrest compared with the negative control small interfering (siNC) groups. Cell apoptosis was promoted by siFGF5 treatment. Cell migration and invasion of H661 and CALU1 cells with siFGF5 transfection were markedly diminished compared with the siNC groups. In addition, migration and invasion‐associated proteins (E‐cadherin, matrix metalloproteinase‐2 [MMP‐2], and MMP‐9) and epithelial mesenchymal transition markers (N‐cadherin, vimentin, snail, and slug) were also regulated by FGF5 siRNA treatment. Gene set enrichment analysis on The Cancer Genome Atlas dataset showed that the Kyoto Encyclopedia of Genes and Genomes (KEGG) cell cycle and vascular endothelial growth factor (VEGF) pathways were correlated with FGF5 expression, which was further confirmed in NSCLC cells by Western blot analysis. Our results indicated that FGF5 silencing suppressed cell growth and invasion via regulation of the cell cycle and VEGF pathways. Therefore, FGF5 may serve as a promising therapeutic strategy for NSCLC.

Hsa_circ_0016760 exacerbates the malignant development of non‑small cell lung cancer by sponging miR‑145‑5p/FGF5

“…High FGF5 expression was an independent prognostic factor for patients, and was associated with worse overall survival and relapse-free survival in lung adenocarcinoma patients. Zhou et al ( 22 ) revealed that FGF5 expression was aberrantly increased in NSCLC tissues and cell lines. The inhibition of FGF5 significantly suppressed NSCLC cell line proliferation, migration and invasion.…”

Validation of MicroRNA-188-5p Inhibition Power on Tumor Cell Proliferation in Papillary Thyroid Carcinoma

“…Metzner demonstrated that the inhibition of FGF5 signaling is associated with reduced melanoma cell proliferation, and anchorage-independent growth 20 . Recently, downregulation of FGF5 has been reported to inhibit cell growth and invasion of human non-small-cell lung cancer cells 9 . In osteosarcoma, miR-567 has been found to inhibit cell proliferation, migration, and invasion by targeting FGF5 21 .…”

“…FGF5 has been demonstrated oncogenic activity of FGF5 in astrocytic brain tumors and attribute to both autocrine effects on the tumor cells as well as paracrine effects on endothelial cells 8 . Zhou et al have demonstrated that the downregulation of FGF5 inhibited cell growth and invasion of human non-small-cell lung cancer cells 9 . FGF5 expression was found to be significantly upregulated in breast cancer patients relative to that in normal controls ( P < 0.0001), and breast cancer patients in the FGF5 low-expression group were correlated with better clinical characteristics 10 .…”

FGF/FGFR Signaling in Hepatocellular Carcinoma: From Carcinogenesis to Recent Therapeutic Intervention

“…FGF5 has been discussed in many other cancers and has multiple roles in cancer development [ 46 , 47 , 48 ]. FGFR1 IIIc and FGFR2 IIIc are considered the preferential receptors for FGF5.…”