EPB49 PROMOTES COLORECTAL CANCER PROLIFERATION, INVASION AND MIGRATION BY REGULATING TIAML-RACL SIGNALING PATHWAY

Zaibo Wen¹, Lurong Huang², Yusheng Chen^{3, *}

¹Department of Gastroenterology, Cangnan People’s Hospital, Cangnan 325800, PR China - ²Department of Ward 25, WenZhou People’s Hospital, Wenzhou 325000, PR China - ³Department of Gastroenterology, Wenzhou Hospital of Traditional Chinese Medicine, Wenzhou 325029, PR China

Objective: To analyze the effect of EPB49 on the proliferation, invasion and migration of colorectal cancer by regulating the Tiaml-Racl signaling pathway. 

Methods: SW480, SW620 and SW490 cells were divided into an overexpression control group and over expression EPB49 group. SW620 cells were divided into an inhibition control group and an inhibition EPB49 group. The overexpression control group and inhibition control group were not treated. The overexpression EPB49 group was given EPB49 multi expression lentivirus vector, and the inhibition group was given EPB49 interference lentivirus vector. The proliferation of rectal cancer cells in each group was detected by the MTT method, the invasion of rectal cancer cells in each group was detected by the Transwell method, and the migration of rectal cancer cells in each group was detected by scratch test. The expression of related proteins in Tiaml-Racl signaling pathway C3, Racl, and other related proteins in rectal cancer cells of each group was analyzed by blot. EPB49 promoted the proliferation, invasion and migration of colorectal cancer by regulating the Tiaml-Racl signaling pathway. 

Results: The growth rate of SW480 cells in the EPB49 overexpression group was significantly lower than that in the control group, and the growth rate of SW620 cells in the EPB49 inhibition group was significantly higher than that in the negative control group (P<.05). Transwell assay showed that the migration and invasion ability of SW480 cells in the EPB49 overexpression group was significantly lower than that in the control group, and the migration and invasion ability of SW620 cells in the EPB49 inhibition group was significantly higher than that in the negative control group (P<.05). Western blot analysis showed that the Racl GTP protein of SW480 cells in the EPB49 overexpression group was significantly lower than that in the control group, and the Racl GTP protein of SW620 cells in the EPB49 inhibition group was significantly higher than that in negative control group (P<.05). 

Conclusion: Overexpression of EPB49 can significantly inhibit the proliferation, migration and invasion of rectal cancer cells; in addition, interference with EPB49 expression can improve the proliferation, migration, and invasion of rectal cancer cells, which may be related to the regulation of Tiaml-Racl signaling pathway related proteins.