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Updated: Jul 10, 2026
14:57
Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
p53: good cop/bad cop
Norman E Sharpless1, Ronald A DePinho
1Department of Adult Oncology, Dana-Farber Cancer Institute, Department of Medicine and Genetics, Harvard Medical School, Boston, MA 02115, USA.
Cell
|August 2, 2002
Summary
The p53 protein, crucial for preventing cancer by halting damaged cell growth, also contributes to aging through DNA damage, telomere shortening, and oxidative stress. Therapies targeting cancer and aging must work around, not on, p53.
Area of Science:
- Molecular Biology
- Gerontology
- Cellular Biology
Background:
- The p53 transcription factor is activated by cellular stresses like DNA damage and oncogene activation.
- p53 initiates gene expression to prevent proliferation of damaged cells, a key anticancer mechanism.
- Emerging evidence suggests p53 activation may negatively impact organismal homeostasis and aging.
Purpose of the Study:
- To discuss the dual role of p53 in cancer suppression and aging.
- To explore the involvement of p53 in major aging theories: DNA damage, telomere shortening, and oxidative stress.
- To position p53 at the intersection of cancer and aging research.
Main Methods:
- Literature review and theoretical discussion.
- Analysis of existing research on p53 function in cellular stress responses.
- Synthesis of data linking p53 to aging pathways.
Main Results:
- p53 plays a significant role in three key theories of human aging.
- These theories include aging mechanisms related to DNA damage, telomere shortening, and oxidative stress.
- p53 exhibits "good cop/bad cop" functions, balancing cancer prevention with aging promotion.
Conclusions:
- p53 is critically positioned at the nexus of opposing forces: cancer and aging.
- Therapeutic strategies to combat cancer and aging must target pathways upstream or downstream of p53.
- Understanding p53's dual role is essential for developing longevity interventions.
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