TMEM206 Promotes EGF-induced Colorectal Cancer EMT Via EGFR-ERK/MAPK-c-Myc Signaling Pathway

Objective: To further clarify the role of TMEM206 in the biological behavior of colorectal cancer(CRC)and explore the possible mechanisms of action.Methods: TMEM206 overexpression plasmid was transfected into human colorectal cancer HCT116 and SW480 cell lines.EGF induced EMT in CRC cells,and the morphology of the cells was observed.The changes of TMEM206 and EMT-related proteins were detected by Western blot.The changes in invasion and migration ability of CRC cells were analyzed by Transwell.Results: Overexpression of TMEM206 promotes EGF-induced EMT-like cell morphology.Western blot analysis showed that TMEM206 overexpression promoted EGF-induced increase in p-ERK and c-Myc protein,and promoted EGF-induced E-cad reduction and increased fibronectin,Zeb1,and snail1/2.Transwell experiments showed that the overexpression of TMEM206 in CRC HCT116 and SW480 cells further promoted the invasion and migration of cells after EGF induction(P<0.05).Conclusion: TMEM206 promotes the progression of CRC by enhancing the interaction between AKT and ERK signaling pathways,and TMEM206 promotes the development of EMT in colorectal cancer,which in turn affects the invasion and metastasis of colorectal cancer.