Correlation between FAK and EGF-Induced EMT in Colorectal Cancer Cells.

Kun Huang,Donglin Bian,Ningning Gao,Xuemei Wang,Qixi Zhai,Puxu Yang,Mingwei Li

doi:10.1155/2020/5428920

Abstract

Epithelial-mesenchymal transition (EMT) plays an important role in the invasion and metastasis of colorectal cancer, which is mediated by FAK and EGF. However, whether FAK participates in EMT in colorectal cancer cells through the EGF/EGFR signaling pathway remains unknown. The aim of this study was to investigate the effector mechanisms of FAK in the process of EGF-induced EMT in colorectal cancer cells and to determine whether miR-217 is involved in this process. Caco-2 cancer cells were routinely cultured with and without treatment with 100 ng/mL EGF, and changes in cell morphology were observed using an inverted microscope. In addition, a transwell assay was used to detect cell migration under the condition of EGF treatment. The expression of FAK, pFAK, E-cadherin, vimentin, and β actin was assessed by western blotting, and the expression of miR-217 was assessed using real-time PCR. We found that EGF induced EMT in colorectal cancer cells and enhanced cell migration and invasion ability. Moreover, FAK was involved in the EGF-induced EMT of colorectal cancer cells. EGF upregulated the expression of E-cadherin in colorectal cancer cells by activating FAK, and miR-217 was found to participate in EGF-induced EMT in colorectal cancer cells. Our findings indicate that EGF induces EMT in colorectal cancer cells by activating FAK, and miR-217 is involved in the EGF/FAK/E-cadherin signaling pathway.

Highlights

Colorectal cancer is a common malignancy of the digestive tract, and the metastasis is the main cause of death in colorectal cancer
There have been no reports far on whether miR-217 is involved in epidermal growth factor (EGF)-induced epithelial-mesenchymal transition (EMT) in colorectal cancer cells. It has not yet been determined whether FAK is involved in the regulation of EMT in colorectal cancer cells through the EGF/EGF receptor (EGFR) signaling pathway. erefore, this study aims to investigate whether FAK is involved in the regulation of colorectal cancer cells through the promotion of EMT via the EGF/EGFR signaling pathway and the enhancement of migration ability
The expression of E-cadherin was significantly reduced after 24 hours of EGF treatment, while the expression of vimentin was significantly elevated

Summary

Introduction

Colorectal cancer is a common malignancy of the digestive tract, and the metastasis is the main cause of death in colorectal cancer. Tumor metastasis is a highly complex process involving multiple factors and steps. Recent studies have shown that epithelial-mesenchymal transition (EMT) plays an important role in tumor invasion and metastasis [1, 2]. E process of EMT includes changes in cell phenotype and changes in cell markers, such as the loss of epithelial cell markers (e.g., E-cadherin) and gain of mesenchymal cell markers (e.g., vimentin and alpha-smooth muscle actin (α-SMA)). Studies have shown that the occurrence of EMT is a complex process involving the tumor microenvironment, growth factors, kinases, transcription factors, and micro-RNAs (miRNAs), but the specific mechanisms underlying this process remain unclear. Many studies are currently carried out to investigate the detailed mechanisms underlying the occurrence of EMT in tumor cells

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