Role of PI3K/Akt pathway in Benzidine-induced proliferation in SV-40 immortalized human uroepithelial cell.

backgroundLong 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.

methodsThe 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.

resultsResults showed that benzidine acted to induce cell proliferation at low doses (P<0.05

conclusionsActivated PI3K/Akt signal pathway promotes benzidine-triggered cell proliferation. It may shed light on the molecular mechanisms that the activated PI3K/Akt pathway promotes benzidine-triggered cell proliferation and intervention of its target.