Modulation of the p53 family network by RNA-binding proteins

Chris Lucchesi, Jin Zhang, Xinbin Chen

Research output: Contribution to journalReview article

3 Citations (Scopus)

Abstract

Since its discovery more than three decades ago, tumor suppressor p53 has been shown to play pivotal roles in both maintaining genomic integrity and tumor suppression. p53 functions as a transcription factor responding to a multitude of cellular stressors, regulating the transcription of many genes involved in cell-cycle arrest, senescence, autophagy, and apoptosis. Extensive work has revealed that p53 is one of the most commonly mutated tumor suppressor genes. The last three decades have demonstrated that p53 activity is controlled through transcriptional regulation and posttranslational modifications. However, evolving work is now uncovering that p53, and other p53 family members, are post-transcriptionally regulated by multiple RNA-binding proteins (RBPs). Understanding the regulation of p53 by RBPs may potentially open up the possibility for cancer therapeutic intervention. This review focuses on the posttranscriptional regulation of p53, and p53 family members, by RNA binding proteins and the reciprocal feedback pathways between several RNA-biding proteins modulating p53, and p53 family members.

Original languageEnglish (US)
Pages (from-to)676-684
Number of pages9
JournalTranslational Cancer Research
Volume5
Issue number6
DOIs
StatePublished - 2016

Fingerprint

RNA-Binding Proteins
Neoplasms
Autophagy
Post Translational Protein Processing
Cell Cycle Checkpoints
Tumor Suppressor Genes
Transcription Factors
RNA
Apoptosis
Genes
Proteins
Therapeutics

Keywords

  • P53
  • Post-transcriptional regulation
  • Rbm38
  • RNA-binding proteins (RBPs)

ASJC Scopus subject areas

  • Oncology
  • Radiology Nuclear Medicine and imaging
  • Cancer Research

Cite this

Modulation of the p53 family network by RNA-binding proteins. / Lucchesi, Chris; Zhang, Jin; Chen, Xinbin.

In: Translational Cancer Research, Vol. 5, No. 6, 2016, p. 676-684.

Research output: Contribution to journalReview article

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