Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5860405 | Toxicology Letters | 2013 | 10 Pages |
Abstract
Nickel compounds have been found to be carcinogenic based upon epidemiological, animal and cell culture studies. Previous studies suggest that epigenetic mechanisms play a role in Nickel-induced carcinogenesis such as DNA methylation and histone modification. In this study, we investigated the role of microRNAs (miRNAs) in nickel-induced carcinogenesis. The expression of several miRNAs which may function as tumor suppressor genes revealed a strong downregulation of miR-203 in Ni3S2-transformed 16HBE cells (NSTCs). Meanwhile, we observed hypermethylation of CpGs in miR-203 promoter and first exon area, and proved that the hyper-methylated miR-203 was involved in the Nickel-induced tumorigenesis. Moreover, we identified that miR-203 may suppress the tumorigenesis at least in part through negatively regulating its target gene ABL1. Our findings indicate that DNA methylation-associated silencing of tumor suppressor miRNAs contributes to the development of Nickel-induced cancer.
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Authors
Jing Zhang, Yang Zhou, You-Jun Wu, Meng-Jie Li, Rui-Jin Wang, Shun-Quan Huang, Rong-Rong Gao, Lin Ma, Hong-Jun Shi, Jun Zhang,