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Updated: Apr 1, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
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PRMT5-dependent p53 escape in tumorigenesis.

Yan Li1, J Alan Diehl1

  • 1Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA.

Oncoscience
|October 2, 2015
PubMed
Summary

Protein arginine methyltransferase 5 (PRMT5) promotes cancer cell survival by modifying wild-type p53. This mechanism helps tumors evade apoptosis, even when p53 is functional.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling

Background:

  • Mutations in p53 signaling are common in human cancers.
  • The mechanisms enabling cancer cells with wild-type p53 to bypass its tumor-suppressive functions are not fully understood.

Purpose of the Study:

  • To investigate the role of PRMT5 in the evasion of wild-type p53 tumor suppression.
  • To elucidate how PRMT5 contributes to cancer cell survival and apoptosis evasion.

Main Methods:

  • Analysis of PRMT5 expression in human cancers.
  • Investigating the interaction between PRMT5, cyclin D1, and p53.
  • Assessing the effect of PRMT5 on p53 arginine methylation.
  • Evaluating the impact of PRMT5-mediated p53 modification on apoptosis.
Keywords:
PRMT5apoptosisarginine methylationoncogenesisp53

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Main Results:

  • PRMT5 is frequently elevated in human cancers.
  • PRMT5 cooperates with oncogenic cyclin D1.
  • PRMT5 mediates arginine methylation of wild-type p53.
  • This modification promotes the bypass of wild-type p53 function, leading to apoptosis evasion.

Conclusions:

  • PRMT5 plays a critical role in enabling cancer cells with functional p53 to evade apoptosis.
  • Targeting PRMT5 may offer a therapeutic strategy for cancers that retain wild-type p53.