Benzidine Induces Epithelial-Mesenchymal Transition of Human Bladder Cancer Cells through Activation of ERK5 Pathway

Molecules and Cells
Xin SunCaiyun Zhong

Abstract

Benzidine, a known carcinogen, is closely associated with the development of bladder cancer (BC). Epithelial-mesenchymal transition (EMT) is a critical pathophysiological process in BC progression. The underlying molecular mechanisms of mitogen-activated protein kinase (MAPK) pathway, especially extracellular regulated protein kinases 5 (ERK5), in regulating benzidine-induced EMT remains unclarified. Hence, two human bladder cell lines, T24 and EJ, were utilized in our study. Briefly, cell migration was assessed by wound healing assay, and cell invasion was determined by Transwell assay. Quantitative PCR and western blot were utilized to determine both gene expressions as well as protein levels of EMT and MAPK, respectively. Small interfering RNA (siRNA) was transfected to further determine ERK5 function. As a result, the migration and invasion abilities were enhanced, epithelial marker expression was decreased while mesenchymal marker expression was increased in human BC cell lines. Meanwhile, benzidine administration led to activation of ERK5 and activator protein 1 (AP-1) proteins, without effective stimulation of the Jun N-terminal kinase (JNK) or p38 pathways. Moreover, Benzidine-induced EMT and ERK5 activation were comple...Continue Reading

Citations

Oct 16, 2019·Molecular Biology Reports·Xiaoyan JiangSongshu Xiao
Mar 25, 2019·International Journal of Molecular Sciences·Barbara Stecca, Elisabetta Rovida
Dec 12, 2020·Nutrition and Cancer·Connor ChestnutShrikant Anant

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BETA
xenografts

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SPSS

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