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Related Experiment Video

Updated: May 24, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

P53 and the proteasome regulate androgen receptor activity.

Natalya V Guseva¹, Oskar W Rokhlin, Rebecca A Glover

¹Department of Pathology, University of Iowa, Iowa City, Iowa, USA. natalya-guseva@uiowa.edu

Cancer Biology & Therapy

|March 13, 2012

Summary

The tumor suppressor p53 influences androgen receptor (AR) activity. Proteasome inhibitors show reduced efficacy in inhibiting AR when p53 is present, suggesting p53 status impacts treatment effectiveness in prostate cancer.

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Yeast As a Chassis for Developing Functional Assays to Study Human P53

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Area of Science:

Molecular Biology
Cancer Research
Biochemistry

Background:

Mutual regulation between p53 and the androgen receptor (AR) is established.
The precise role of p53 in modulating AR expression and activity requires further elucidation, particularly in the context of prostate cancer.

Purpose of the Study:

To investigate how p53 influences androgen receptor (AR) expression and activity.
To determine the role of p53 in proteasome-dependent inhibition of AR activity.

Main Methods:

Utilized ARE-Luciferase reporter assays in LNCaP and PC3 cell lines with varying p53 and AR statuses.
Quantitatively assessed AR activity following treatment with proteasome inhibitors (lactacystin).
Measured AR-DNA binding affinity in response to proteasome inhibition.

Main Results:

p53 expression decreased DHT-dependent activity of wild-type AR.
Proteasome inhibitor lactacystin significantly inhibited AR activity and AR-DNA binding in LNCaP cells.
LNCaP-sip53 transfectants showed no inhibition of AR activity or AR-DNA binding by lactacystin.
The inhibitory effects of proteasome inhibitors on AR activity are dependent on p53 status.

Conclusions:

p53 status is a critical determinant of the efficacy of proteasome inhibitors in modulating AR activity in prostate cancer.
Further investigation into the role of p53 in tumors treated with proteasome inhibitors is warranted.