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논문 기본 정보

자료유형
학술저널
저자정보
Xin Sun (The Second Affiliated Hospital of Anhui Medical University) Tao Zhang (The Second Affiliated Hospital of Anhui Medical University) Qifei Deng (Anhui Provincial Children’s Hospital) Qirui Zhou (The Second Affiliated Hospital of Anhui Medical University) Xianchao Sun (The Second Affiliated Hospital of Anhui Medical University) Enlai Li (The Second Affiliated Hospital of Anhui Medical University) Dexin Yu (The Second Affiliated Hospital of Anhui Medical University) Caiyun Zhong (Nanjing Medical University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제41권 제3호
발행연도
2018.3
수록면
188 - 197 (10page)
DOI
10.14348/molcells.2018.2113

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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 ex-pression 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 completely suppressed by XMD8-92 and siRNAs specific to ERK5. Of note, ERK1/2 was acti-vated in benzidine-treated T24 cells, while benzidine-induced EMT could not be reversed by U0126, an ERK1/2 inhibitor, as indicated by further study. Collectively, our findings revealed that ERK5-mediated EMT was critically involved in benzidine-correlated BC progression, indicating the therapeutic significance of ERK5 in benzidine-related BC.
#benzidine #bladder cancer #epithelial-mesenchymal transition #ERK5

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참고문헌 (33)

참고문헌 신청
Bakiri, L. / 2015 / Fra-1/AP-1 induces EMT in mammary epithelial cells by modulating Zeb1/2 and $TGF{\beta}$ expression / Cell Death Differ. 22:336~350 Crossref Baan, R. / 2008 / Carcinogenicity of some aromatic amines, organic dyes, and related exposures / Lancet Oncol. 9:322~323 Crossref Boffetta, P. / 2008 / Tobacco smoking and risk of bladder cancer / Scand J. Urol. Nephrol. Suppl. 218:45~54 google schola Chung, K.T. / 2016 / Azo dyes and human health: A review / J. Environ. Sci. Health C. Environ. Carcinog. Ecotoxicol. Rev. 34:233~261 Crossref Geng, H. / 2015 / ERK5 positively regulates cigarette smoke-induced urocystic epithelial-mesenchymal transition in SV-40 immortalized human urothelial cells / Oncol Rep. 34:1581~1588 Crossref

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