@article{TCR30468,
author = {Demao Ding and Zhiqi Liu and Li Zhao and Hao Geng and Zhaofeng Liang and Dexin Yu},
title = {Role of PI3K/Akt pathway in Benzidine-induced proliferation in SV-40 immortalized human uroepithelial cell},
journal = {Translational Cancer Research},
volume = {8},
number = {4},
year = {2019},
keywords = {},
abstract = {Background: Long term exposure to benzidine has been determined as a cause of urothelial carcinoma. But how it works in the process of cell proliferation that involves in tumor growth is not examined yet. In the current research, the effect of PI3K/Akt on cell proliferation mediated by benzidine was confirmed.
Methods: The immortalized SV-40 human uroepithelial cells (SV-HUC-1) had been subjected to 6 days of benzidine treatment at various contents, then MTT assay, together with subsequent flow cytometry assay were used for observing effects on cell proliferation. Further Western blots were used to detect the expression of total-Akt, phospho-Akt and specific proteins of cell cycle. The Akt, Cyclin D1, PCNA and P21 mRNA levels were detected through RT-PCR. In addition, the blocker-LY294002 was used to cut down the PI3K/Akt signaling pathway. And then those parameters were detected using the same methods as above.
Results: Results showed that benzidine acted to induce cell proliferation at low doses (P},
issn = {2219-6803}, url = {https://tcr.amegroups.org/article/view/30468}
}