Loss of p53 activates thyroid hormone via type 2 deiodinase and enhances dna damage

HIGHLIGHTS

SUMMARY

    Conversely, even partial loss of p53 elevates D2/TH resulting in stimulation and increased fitness of tumor cells by boosting a significant transcriptional program leading to modulation of genes involved in DNA damage and repair and redox signaling. This region contains several binding_sites for transcription factors, including 15 different decameric half-sites, with a consensus motif RRRCWWGYYY, recognized by the tumor suppressor p53 (Fig 1a and Supplementary Fig 1). To explore the possibility that p53 may be directly involved in the regulation of DIO2 gene_expression, SCC cancer cells were transfected with a wild-type . . .

     

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