ECT2 promotes proliferation and metastasis of esophageal squamous cell carcinoma via the RhoA-ERK signaling pathway

• Published in: European review for medical and pharmacological sciences Vol. 24; no. 15; p. 7991
• Main Authors: Sun, B-Y, Wei, Q-Q, Liu, C-X, Zhang, L, Luo, G, Li, T, Lü, M-H
• Format: Journal Article
• Language: English
• Published: Italy 01.08.2020
• Subjects: Animals; Cell Movement; Cell Proliferation; Esophageal Neoplasms - metabolism; Esophageal Neoplasms - pathology; Esophageal Squamous Cell Carcinoma - metabolism; Esophageal Squamous Cell Carcinoma - pathology; Humans; MAP Kinase Signaling System; Mice; Neoplasms, Experimental - metabolism; Neoplasms, Experimental - pathology; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins - metabolism; rhoA GTP-Binding Protein - metabolism; Tumor Cells, Cultured
• ISSN: 2284-0729
• DOI: 10.26355/eurrev_202008_22482

In this study, the effect of epithelial cell transformation sequence 2 (ECT2) on the proliferation, invasion and migration of esophageal squamous cell carcinoma (ESCC) was investigated by interfering the expression of ECT2. Interfering with the expression level of ECT2 in human squamous cell carcinomas KYSE140 and EC9706 cell lines, the changes of KYSE140 and EC9706 cell proliferation, invasion, and migration were measured using the CCK-8 method, transwell test, and scratch test, respectively. The effects of ECT2 on the Ras homolog gene family, member A-extracellular regulated protein kinases (RhoA-ERK) signaling pathway were also observed. Compared with the control group, the proliferation, migration, and invasion ability of EC9706 and KYSE140 cells after ECT2 knockout were significantly reduced (p <0.05). The knockdown of ECT2 expression in ESCC cell lines suppressed the activation of RhoA-ERK signaling pathway and protein expression of VEGF and MMP9. ECT2 could regulated the expression of VEGF and MMP9 to inhibit cells proliferation, invasion, migration and tumor development through RhoA-ERK signaling pathway. Therefore, ECT2 could be an available marker, and provide a new theoretical basis for the treatment of ESCC.