Related Experiment Video
Updated: Jun 14, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
Targeting the p53-family in cancer and chemosensitivity: triple threat
1Cell Biology Program, Hospital for Sick Children Research Institute, Toronto, Ontario, M5G 1L7, Canada.
Abstract:
The p53-family of transcription factors consists of three genes - p53, p63, and p73 - that share significant structural and functional similarities. Although these genes encode multiple variants that have opposing functions in cancer biology, the full-length, transactivating (TA) p53-family members are potent inducers of apoptosis and tumor suppression. Many anti-cancer agents, from traditional chemo- and radiation therapies to more recently developed small molecules, exert their effects by enhancing the anti-proliferative effects of p53 and TAp63/p73. In this review, we provide an overview of the regulatory pathways controlling the p53-family proteins as a framework for understanding p53-family targeted drug mechanisms. We will also summarize recent work on promising attempts to re-activate p53 in tumors. In addition, we will discuss how p63 and p73 - the two more recently discovered p53-family members - have affected drug discovery and how these two genes may also hold promise as drug targets for recent and future novel therapies. This review will emphasize how targeting multiple members of the family of p53 proteins is likely to provide an increased threat to the growth of cancer cells.
Insights
The p53-family proteins (p53, p63, p73) are key in cancer suppression by inducing apoptosis. Targeting these proteins and their variants offers promising anti-cancer drug strategies.
Area of Science:
- Molecular Biology
- Cancer Biology
- Drug Discovery
Background:
- The p53-family comprises p53, p63, and p73, sharing structural and functional similarities.
- These genes produce variants with opposing roles in cancer, but full-length transactivating (TA) members induce apoptosis and suppress tumors.
- Many anti-cancer agents enhance the anti-proliferative effects of p53 and TAp63/p73.
Purpose of the Study:
- To review regulatory pathways of p53-family proteins for understanding drug mechanisms.
- To summarize recent efforts in reactivating p53 in tumors.
- To discuss the impact of p63 and p73 on drug discovery and their potential as therapeutic targets.
Main Methods:
- Literature review of p53-family regulatory pathways.
- Analysis of current research on p53 reactivation strategies.
- Examination of the role of p63 and p73 in anti-cancer drug development.
Main Results:
- p53-family proteins are crucial regulators of apoptosis and tumor suppression.
- Targeting p53-family members is a key mechanism for many anti-cancer therapies.
- p63 and p73 present novel opportunities as drug targets.
Conclusions:
- Understanding p53-family regulation is essential for developing targeted cancer therapies.
- Reactivating p53 and targeting p63/p73 show significant promise for novel anti-cancer treatments.
- Simultaneously targeting multiple p53-family members may enhance anti-cancer efficacy.
Related Concept Videos
Abnormal Proliferation
DNA Damage can Stall the Cell Cycle
DNA Damage Can Stall the Cell Cycle
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Treatment Resistant Cancers

