Benzidine induces epithelial-mesenchymal transition in human uroepithelial cells through ERK1/2 pathway

Biochemical and Biophysical Research Communications
Li ZhaoCai-Yun Zhong

Abstract

Prolonged benzidine exposure is a known cause of urothelial carcinoma (UC). Benzidine-induced epithelial-to-mesenchymal transition (EMT) is critically involved in cell malignant transformation. The role of ERK1/2 in regulating benzidine-triggered EMT has not been investigated. This study was to investigate the regulatory role of ERK1/2 in benzidine-induced EMT. By using wound healing and transwell chamber migration assays, we found that benzidine could increase SV-HUC-1 cells invasion activity, western blotting and Immunofluorescence showed that the expression levels of Snail, β-catenin, Vimentin, and MMP-2 were significantly increased, while, the expression levels of E-cadherin, ZO-1 were decreased. To further demonstrate the mechanism in this process, we found that the phosphorylation of ERK1/2, p38, JNK and AP-1 proteins were significantly enhanced compared to the control group (*P < 0.05). Afterward, treated with MAPK pathways inhibitors, only ERK inhibitor(U0126)could reduce the expression of EMT markers in SV-HUC-1 cells, but not p38 and JNK inhibitor(SB203580, SP600125), which indicated that benzidine induces the epithelial-mesenchymal transition in human uroepithelial cells through ERK1/2 pathway. Taken together, findin...Continue Reading

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Citations

Jan 19, 2016·Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Für Toxikologische Pathologie·Xin SunCai-Yun Zhong
Jan 1, 2016·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Banu IskenderHalit Canatan
Dec 26, 2016·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Xin SunCaiyun Zhong
Nov 24, 2020·International Immunopharmacology·Xin WangQingjiang Jin

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