Knockdown of VASH2 inhibits the stemness and EMT process by regulating ZEB2 in colorectal cancer.

Abstract

VASH2 is associated with the malignant progression of a variety of tumors, but the role and mechanism of VASH2 in colorectal cancer are still unclear. We analyzed the expression of VASH2 in colorectal cancer from the TCGA database and also analyzed the relationship between VASH2 expression and survival of colorectal cancer patients in the PrognoScan database. We verified the role of VASH2 in colorectal cancer through transfecting si-VASH2 into colorectal cancer cells and detecting cell viability by CCK8, cell migration by wound healing assay, and cell invasion by Transwell assay. ZEB2, Vimentin, and E- cadherin protein expression were examined by Western-Blot assay. Cell sphere-forming ability was determined by sphere formation assay, and we further confirmed the mechanism of VASH2 in colorectal cancer progression by rescue assays. Colorectal cancer has a high expression of VASH2, and its expression is associated with a poorer patient survival rate. The vitality, migration, invasion, EMT, and tumor stemness of colorectal cancer cells were all decreased by VASH2 knockdown. These alternations were attenuated by ZEB2 overexpression. Our experiments confirmed that VASH2 affects colorectal cancer cell proliferation, migration, invasion, EMT, and seed bovine stemness by regulating ZEB2 expression.