Low dose arsenite confers resistance to UV induced apoptosis via p53-MDM2 pathway in ketatinocytes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-08-07

AUTHORS

Y Zhou, W Zeng, M Qi, Y Duan, J Su, S Zhao, W Zhong, M Gao, F Li, Y He, X Hu, X Xu, X Chen, C Peng, J Zhang

ABSTRACT

Chronic arsenite and ultraviolet (UV) exposure are associated with skin tumor. To investigate the details by low concentrations of arsenite and UV induced carcinogenesis in skin, hTERT-immortalized human keratinocytes were used as a cellular model with exposure to low concentrations of sodium arsenite and UV. The effect of NaAsO2 on UV treatment-induced apoptosis was measured by flow cytometry and Hoechst staining. We found that the cell apoptosis induced by UV exposure was significantly attenuated after exposure to low-dose arsenite, and knockdown of p53 could block UV-induced apoptosis indicating that this phenomenon depended on p53. Interestingly, the expression of murine double minute 2 (MDM2), including its protein and transcriptional levels, was remarkably high after exposure to low-dose arsenite. Moreover, low-dose arsenite treatment dramatically decreased the MDM2 gene promoter activity, suggesting that this effect has been mediated through transcription. In addition, treatment of PD98059 reversed low-dose arsenite-induced MDM2 expression, and the inhibition of ERK2 expression could significantly block MDM2 expression as a consequence, and p53 expression automatically was increased. To validate the role of p53 in exposure to low-dose arsenite, the expression of p53 was examined by immunohistochemistry in the skin of Sprague−Dawley rats model by chronic arsenite exposure for 6 months and in patients with arsenic keratosis, and the results showed that the expression of p53 was decreased in those samples. Taken together, our results demonstrated that low-dose arsenite-induced resistance to apoptosis through p53 mediated by MDM2 in keratinocytes. More... »

PAGES

e370-e370

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    http://scigraph.springernature.com/pub.10.1038/oncsis.2017.67

    DOI

    http://dx.doi.org/10.1038/oncsis.2017.67

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1091081263

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28785074


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