B-Myb Induces APOBEC3B Expression Leading to Somatic Mutation in Multiple Cancers View Full Text


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Article Info

DATE

2017-03-09

AUTHORS

Wen-Cheng Chou, Wei-Ting Chen, Chia-Ni Hsiung, Ling-Yueh Hu, Jyh-Cherng Yu, Huan-Ming Hsu, Chen-Yang Shen

ABSTRACT

The key signature of cancer genomes is the accumulation of DNA mutations, the most abundant of which is the cytosine-to-thymine (C-to-T) transition that results from cytosine deamination. Analysis of The Cancer Genome Atlas (TCGA) database has demonstrated that this transition is caused mainly by upregulation of the cytosine deaminase APOBEC3B (A3B), but the mechanism has not been completely characterized. We found that B-Myb (encoded by MYBL2) binds the A3B promoter, causing transactivation, and this is responsible for the C-to-T transitions and DNA hypermutation in breast cancer cells. Analysis of TCGA database yielded similar results, supporting that MYBL2 and A3B are upregulated and putatively promote C-to-T transitions in multiple cancer types. Moreover, blockade of EGF receptor with afatinib attenuated B-Myb-A3B signaling, suggesting a clinically relevant means of suppressing mutagenesis. Our results suggest that B-Myb-A3B contributes to DNA damage and could be targeted by inhibiting EGF receptor. More... »

PAGES

44089

References to SciGraph publications

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    URI

    http://scigraph.springernature.com/pub.10.1038/srep44089

    DOI

    http://dx.doi.org/10.1038/srep44089

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1084131989

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28276478


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