Correlation between FAK and EGF-Induced EMT in Colorectal Cancer Cells
Correlation between FAK and EGF-Induced EMT in Colorectal Cancer Cells
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DOI：
10.1155/2020/5428920
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发表时间：
2020-02-17
影响因子：
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通讯作者：
Wang, Xuemei
中科院分区：
文献类型：
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作者：
Huang, Kun;Gao, Ningning;Wang, Xuemei
上皮-间质转化（Epithelial-mesenchymal transition，EMT）在大肠癌的侵袭和转移中起重要作用，其介导机制主要是FAK和EGF。然而，FAK是否通过EGF/EGFR信号通路参与结直肠癌细胞的EMT尚不清楚。本研究的目的是探讨FAK在EGF诱导的大肠癌细胞EMT过程中的效应机制，并确定miR-217是否参与了这一过程。常规培养Caco-2癌细胞，用100 ng/mL EGF处理和不处理，并使用倒置显微镜观察细胞形态的变化。此外，使用transwell分析来检测EGF处理条件下的细胞迁移。通过蛋白质印迹法评估FAK、pFAK、E-cadherin、波形蛋白和β肌动蛋白的表达，并使用实时PCR评估miR-217的表达。我们发现EGF诱导大肠癌细胞发生EMT，并增强细胞的迁移和侵袭能力。此外，FAK参与EGF诱导的大肠癌细胞EMT。EGF通过激活FAK上调大肠癌细胞中E-cadherin的表达，miR-217参与EGF诱导的大肠癌细胞EMT。我们的研究结果表明，EGF通过激活FAK诱导结直肠癌细胞的EMT，而miR-217参与EGF/FAK/E-cadherin信号通路。
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 beta 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.