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Updated: May 23, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
Regulation of p53 stability and apoptosis by a ROR agonist
Yongjun Wang1, Laura A Solt, Douglas J Kojetin
1The Scripps Research Institute, Jupiter, Florida, United States of America.
Abstract:
Activation of p53 function leading to cell-cycle arrest and/or apoptosis is a promising strategy for development of anti-cancer therapeutic agents. Here, we describe a novel mechanism for stabilization of p53 protein expression via activation of the orphan nuclear receptor, RORα. We demonstrate that treatment of cancer cells with a newly described synthetic ROR agonist, SR1078, leads to p53 stabilization and induction of apoptosis. These data suggest that synthetic ROR agonists may hold utility in the treatment of cancer.
Insights
Activating the RORα receptor with SR1078 stabilizes p53 protein, inducing cancer cell death. This discovery offers a new therapeutic strategy targeting RORα for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- p53 protein activation is a key strategy for anti-cancer drug development.
- The orphan nuclear receptor RORα's role in cancer is not fully understood.
Purpose of the Study:
- To investigate a novel mechanism for p53 stabilization through RORα activation.
- To evaluate the anti-cancer potential of synthetic ROR agonists.
Main Methods:
- Treatment of cancer cells with the synthetic ROR agonist SR1078.
- Analysis of p53 protein levels and apoptosis induction.
Main Results:
- SR1078 treatment led to significant p53 protein stabilization.
- SR1078 effectively induced apoptosis in cancer cells.
Conclusions:
- Activation of RORα by synthetic agonists like SR1078 represents a novel pathway for cancer therapy.
- Synthetic ROR agonists show promise as anti-cancer agents by stabilizing p53.
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