Ezrin as a prognostic indicator regulates colon adenocarinoma progression through glycolysis. Issue 3 (16th August 2020)

• Record Type: Journal Article
• Authors: Wang, Yixuan; Yang, Yang; Wang, Xinyue; Jin, Tiefeng; Zhu, Guang; Lin, Zhenhua
• Other Names: Ahn Sang Hoon guestEditor.
• Is Part Of: Journal of gastroenterology and hepatology. Volume 36:Issue 3(2021)
• Page Start: 710
• Page End: 720
• Publication Date: 2020-08-16
• Subjects: Colon adenocarcinoma -- Ezrin -- Glycolysis -- Migration -- Proliferation; Gastroenterology -- Periodicals; Digestive organs -- Diseases -- Periodicals; Liver -- Diseases -- Periodicals; Gastroenterology -- Periodicals; Liver Diseases -- Periodicals; 616.33
• DOI: 10.1111/jgh.15195
• Languages: English
• ISSNs: 0815-9319

Abstract

Abstract: Background and Aim: Aerobic glycolysis (the Warburg effect) is a distinctive metabolic hallmark of colon adenocarcinoma. Ezrin was a member of the Ezrin–Radixin–Moesin protein family and has been found profoundly implicated in tumorigenesis. However, the specific functional roles of Ezrin in metabolic reprogramming of colon adenocarcinoma remain poorly characterized and need to be explored. Methods: The expression of Ezrin in colon adenocarcinoma tissues was screened by bioinformatics analysis and immunohistochemical assay. Si‐RNA‐mediated transfection and overexpression plasmid transfection were performed in colon adenocarcinoma cells. The proliferation viability was measured using MTT, colony formation, and EdU assays. The migration ability was determined using wound healing and transwell assay. The expression of EMT markers and transcriptional factors was detected using immunofluorescence staining and western blot assays. Glucose uptake, lactate production, and ATP assay were performed to validate the effect of Ezrin on glycolysis‐mediated colon adenocarcinoma progression. Results: Ezrin was upregulated in colon adenocarcinoma tissues and associated with poor survival. Ezrin stimulated colon adenocarcinoma cell proliferation, migration, and the process of EMT. Ezrin aroused significant increase in glucose uptake, lactate production, and ATP level in colon adenocarcinoma cells. Further investigations demonstrated that treatment with a glycolytic inhibitor 2‐deoxy‐d ‐glucose reversed the effects reduced by Ezrin on colon adenocarcinoma cells. Conclusions: Our results evidenced a novel mechanism for colon adenocarcinoma cells proliferation and migration induced by Ezrin via glycolysis.