背景:VASH2与多种肿瘤的恶性进展有关,但VASH2在大肠癌中的作用及机制尚不清楚。
方法:我们从TCGA数据库分析了VASH2在结直肠癌中的表达,并在PrognoScan数据库中分析了VASH2表达与结直肠癌患者生存之间的关系。我们通过将si-VASH2转染到结直肠癌细胞中并通过CCK8检测细胞活力,通过伤口愈合试验检测细胞迁移,验证了VASH2在结直肠癌中的作用。通过Transwell分析和细胞侵袭。ZEB2Vimentin,通过Western-Blot检测E-钙黏着蛋白的表达。通过球体形成测定确定细胞球体形成能力,我们通过挽救试验进一步证实了VASH2在结直肠癌进展中的作用机制。
结果:结直肠癌中VASH2的高表达,其表达与患者生存率较差相关。活力,迁移,入侵,EMT,VASH2敲除后,结直肠癌细胞的肿瘤干性均降低。这些交替通过ZEB2过表达减弱。
结论:我们的实验证实VASH2影响结直肠癌细胞增殖,迁移,入侵,EMT,通过调节ZEB2的表达和种子牛的干性。
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: Our experiments confirmed that VASH2 affects colorectal cancer cell proliferation, migration, invasion, EMT, and seed bovine stemness by regulating ZEB2 expression.