Hyper-methylated miR-203 dysregulates ABL1 and contributes to the nickel-induced tumorigenesis |
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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 |
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Institution: | 1. Translational Center for Stem Cell Research, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China;2. School of Life Science and Technology, Tongji University, Shanghai 200092, China;3. Department of Regenerative Medicine, Tongji University School of Medicine, Shanghai 200092, China |
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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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Keywords: | NSTCs Ni3S2-transformed 16HBE cells |
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