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Environmental toxicology

Low concentration arsenite activated JAK2/STAT3 signal and increased proliferative factor expressions in SV-HUC-1cells after short and long time treatment.


PMID 28444938

Abstract

Epidemiological studies have indicated that ingestion of inorganic arsenic resulted in increased risks of bladder cancer and chronic hyperproliferation could play a direct role in the development of cancer. This study examined the effects of arsenite on JAK2/STAT3 pathway and expressions of proliferation and anti-apoptosis factors. The results showed that long term exposure to low doses arsenite enhanced human uroepithelial cells (SV-HUC-1 cells) proliferation and BrdU positive rate was significant increased. mRNA and protein expressions of proliferation factors, such as cyclin D1, COX-2, and proliferating cell nuclear antigen (PCNA), increased in chronically exposed arsenite SV-HUC-1 cells with exposure time. Furthermore, JAK2/STAT3 signal pathway was activated following exposure to arsenite in SV-HUC-1 cells. Knockdown of STAT3 reduced expressions of cyclin D1, COX-2, PCNA, and BCL2 induced by arsenite. In conclusion, arsenic induced proliferation in human uroepithelial cells after short and long term exposure to arsenite and JAK2/STAT3 signaling pathway might be pivotal in arsenite-induced proliferation by regulating cyclin D1, COX-2, PCNA, and BCL2.