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Coordinate transcriptional and translational repression of p53 by TGF-β1 impairs the stress response.

Abstract：

:Cellular stress results in profound changes in RNA and protein synthesis. How cells integrate this intrinsic, p53-centered program with extracellular signals is largely unknown. We demonstrate that TGF-β1 signaling interferes with the stress response through coordinate transcriptional and translational repression of p53 levels, which reduces p53-activated transcription, and apoptosis in precancerous cells. Mechanistically, E2F-4 binds constitutively to the TP53 gene and induces transcription. TGF-β1-activated Smads are recruited to a composite Smad/E2F-4 element by an E2F-4/p107 complex that switches to a Smad corepressor, which represses TP53 transcription. TGF-β1 also causes dissociation of ribosomal protein RPL26 and elongation factor eEF1A from p53 mRNA, thereby reducing p53 mRNA association with polyribosomes and p53 translation. TGF-β1 signaling is dominant over stress-induced transcription and translation of p53 and prevents stress-imposed downregulation of Smad proteins. Thus, crosstalk between the TGF-β and p53 pathways defines a major node of regulation in the cellular stress response, enhancing drug resistance.

journal_name

Mol Cell

journal_title

Molecular cell

authors

López-Díaz FJ,Gascard P,Balakrishnan SK,Zhao J,Del Rincon SV,Spruck C,Tlsty TD,Emerson BM

doi

10.1016/j.molcel.2013.04.029

subject

Has Abstract

pub_date

2013-05-23 00:00:00

pages

552-64

issue

4

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(13)00334-1

journal_volume

50

pub_type

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