Huang Kun, Gao Ningning, Bian Donglin, Zhai Qixi, Yang Puxu, Li Mingwei, Wang Xuemei
Department of Ultrasonic Diagnosis, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
J Oncol. 2020 Feb 17;2020:5428920. doi: 10.1155/2020/5428920. eCollection 2020.
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 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.
上皮-间质转化（EMT）在结直肠癌的侵袭和转移中起重要作用，其由黏着斑激酶（FAK）和表皮生长因子（EGF）介导。然而，FAK是否通过EGF/表皮生长因子受体（EGFR）信号通路参与结直肠癌细胞的EMT仍不清楚。本研究的目的是探讨FAK在EGF诱导的结直肠癌细胞EMT过程中的效应机制，并确定微小RNA-217（miR-217）是否参与此过程。将Caco-2癌细胞常规培养，分别给予或不给予100 ng/mL EGF处理，用倒置显微镜观察细胞形态变化。此外，采用Transwell实验检测EGF处理条件下的细胞迁移情况。通过蛋白质免疫印迹法评估FAK、磷酸化FAK、E-钙黏蛋白、波形蛋白和肌动蛋白的表达，采用实时定量聚合酶链反应评估miR-217的表达。我们发现，EGF诱导结直肠癌细胞发生EMT，并增强细胞迁移和侵袭能力。此外，FAK参与EGF诱导的结直肠癌细胞EMT。EGF通过激活FAK上调结直肠癌细胞中E-钙黏蛋白的表达，且发现miR-217参与EGF诱导的结直肠癌细胞EMT。我们的研究结果表明，EGF通过激活FAK诱导结直肠癌细胞发生EMT，且miR-217参与EGF/FAK/E-钙黏蛋白信号通路。
