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Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

Androgen receptor drives cellular senescence.

Yelena Mirochnik1, Dorina Veliceasa, Latanya Williams

  • 1Urology Department, Northwestern University, Chicago, Illinois, United States of America.

Plos One
|March 10, 2012
PubMed
Summary

Androgen receptor (AR) can suppress prostate cancer by inducing cell senescence. This study reveals AR-driven senescence involves p21, p63, reactive oxygen species (ROS), and Rb, independent of p53.

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Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • The androgen receptor (AR) typically promotes prostate cancer progression.
  • However, AR also exhibits tumor-suppressive effects, but the mechanisms are unclear.

Purpose of the Study:

  • To elucidate the mechanisms behind the anti-cancer effects of AR, specifically its role in inducing cell senescence.
  • To investigate the molecular pathways involved in AR-driven senescence.

Main Methods:

  • Investigated AR-driven senescence in prostate cancer cells in vitro and in vivo.
  • Utilized p21 and p63 knockdown, ROS quenching (N-Acetyl cysteine), and p63 silencing.
  • Examined the role of Rb phosphorylation and PML tumor suppressor localization.

Main Results:

  • AR activation induced p53-independent senescence by upregulating p21, which reduced p63.
  • AR also increased ROS, suppressing Rb phosphorylation, a key senescence pathway.
  • These pathways, involving PML, converged to cause growth arrest and senescence, even with high mTOR activity and absent p53.

Conclusions:

  • This study demonstrates for the first time that a nuclear hormone receptor, AR, can induce cell senescence.
  • AR's anti-cancer activity is mediated through novel p53-independent pathways involving p21, p63, ROS, Rb, and PML.