The function of FAK/CCDC80/E‑cadherin pathway in the regulation of B16F10 cell migration

Pei,Guoshun; Lan,Yan; Lu,Weijie; Ji,Lina; Hua,Zi‑Chun

doi:10.3892/ol.2018.9159

The function of FAK/CCDC80/E‑cadherin pathway in the regulation of B16F10 cell migration

Authors:
- Guoshun Pei
- Yan Lan
- Weijie Lu
- Lina Ji
- Zi‑Chun Hua
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Affiliations: The State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu 210046, P.R. China
Published online on: July 17, 2018 https://doi.org/10.3892/ol.2018.9159
Pages: 4761-4767

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Abstract

Focal adhesion kinase (FAK) is a non‑receptor tyrosine kinase involved in the development and progression of cancer. However, the regulatory role of FAK in cell migration remains unclear. The aim of the present study was to investigate the mechanism underlying the regulation of melanoma cell migration by FAK. The effect of FAK knockdown on gene expression in B16F10 cells was examined by gene chip analysis. The expression levels of coiled‑coil domain containing 80 (CCDC80) and epithelial (E)‑cadherin were analyzed by reverse transcription quantitative polymerase chain reaction and western blotting. Wound healing and transwell assays were used to monitor B16F10 cell migration. It was identified that the knockdown of FAK increased the expression levels of CCDC80 and E‑cadherin, while the overexpression of CCDC80 elevated E‑cadherin expression. Concurrently, upregulation of CCDC80 inhibited the migration of B16F10 cells, and downregulation of CCDC80 promoted the migration of B16F10 cells. The clinical data from the Oncomine database also revealed that the mRNA level of FAK was increased while the mRNA levels of CCDC80 and E‑cadherin were decreased in patients with melanoma compared with normal controls. Taken together, the results of the present study suggest that the regulation of B16F10 melanoma cell migration by FAK is potentially mediated by CCDC80.

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