Jordan Ashley, Zhang Xiaoru, Li Jinquan, Laulicht-Glick Freda, Sun Hong, Costa Max
Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York, United States of America.
Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY, United States of America.
PLoS One. 2017 Mar 17;12(3):e0173624. doi: 10.1371/journal.pone.0173624. eCollection 2017.
Both nickel and cadmium compounds have been established as group I carcinogens for several decades. Despite over-whelming evidence of these compounds' carcinogenicity in humans, the specific underlying molecular mechanisms that govern metal induced cellular transformation remain unclear. In this study, we found that there were slightly different effects on decreased SLBP mRNA and protein as well as increased polyA H3.1 in our nickel exposed cells. This suggested that nickel and arsenic have similar effects on canonical histone mRNA transcription and translation. We also saw that the depletion of SLBP protein was reversed by inhibiting the proteosome. Finally, we showed that inhibiting the SLBP mRNA and protein levels were rescued by epigenetic modifiers suggesting that nickel's effects on SLBP may be mediated via epigenetic mechanisms. Taken together these results suggest a similar mechanism by which both arsenic and nickel may exert their carcinogenic effects.
几十年来,镍和镉化合物均已被确认为第1类致癌物。尽管有大量证据表明这些化合物对人类具有致癌性,但控制金属诱导细胞转化的具体潜在分子机制仍不清楚。在本研究中,我们发现,在镍暴露细胞中,SLBP mRNA和蛋白水平降低以及多聚腺苷酸化H3.1增加的影响略有不同。这表明镍和砷对经典组蛋白mRNA转录和翻译具有相似的影响。我们还发现,通过抑制蛋白酶体可逆转SLBP蛋白的耗竭。最后,我们表明,表观遗传修饰剂可挽救SLBP mRNA和蛋白水平的抑制,这表明镍对SLBP的影响可能通过表观遗传机制介导。综上所述,这些结果提示了砷和镍可能发挥致癌作用的相似机制。