Suppression of LINC00460 mediated the sensitization of HCT116 cells to ionizing radiation by inhibiting epithelial–mesenchymal transition. Issue 2 (24th April 2020)

• Record Type: Journal Article
• Authors: Zhang, Jiani; Ding, Lixin; Sun, Gaofeng; Ning, Huacheng; Huang, Ruixue
• Is Part Of: Toxicology research. Volume 9:Issue 2(2020)
• Page Start: 107
• Page End: 116
• Publication Date: 2020-04-24
• Subjects: radiation -- lncRNA -- cancer; Toxicology -- Periodicals; 615.9005
• DOI: 10.1093/toxres/tfaa010
• Languages: English
• ISSNs: 2045-452X

Abstract

Abstract: Radiation resistance is the most common challenge for improving radiotherapy. The mechanisms underlying the development of radioresistance remain poorly understood. This study aims to explore the role of LINC00460 in ionizing radiation-induced radioresistance as well as the mechanisms by which LINC00460 is regulated by radiation exposure. The expression of LINC00460 was measured. Cell proliferation and colony formation were measured in HCT116 cells after treatment by radiation. The development of epithelial–mesenchymal transition (EMT) was determined with or without knockdown LINC00460 expression using western blot analysis. Transcription activity was determined using a series of LINC00460-promoter luciferase reporter gene vectors. LINC00460 expression was significantly higher in HCT116 cells, relative to other cell types, with LINC00460 expression significantly affecting HCT116 cell proliferation. Suppression of LINC00460 inhibits EMT development in HCT116 cells via regulation of ZEB1 expression. Furthermore, LINC00460 expression was induced by irradiation via the activation of c-jun transcription factor-binding element located on the LINC00460 promoter. LINC00460 was shown to play a crucial role in EMT-associated progression of colorectal cancer, indicating that LINC00460 may be an indicator or new potential therapeutic target for colorectal cancer radiosensitization.