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Caught in the cross fire: p53 in inflammation
Tomer Cooks1, Curtis C Harris2, Moshe Oren3
1Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD 20892-4258, USA and Molecular Cell Biology, Weizmann Institute for Science, Rehovot 76100, Israel tomer.cooks@nih.gov.
Carcinogenesis
|June 20, 2014
Summary
The p53 tumor suppressor protein maintains genome stability and cellular homeostasis. It also interacts with inflammation, influencing chronic inflammation and cancer development based on its status.
Area of Science:
- Molecular Biology
- Oncology
- Immunology
Background:
- The p53 transcription factor is a critical tumor suppressor involved in genome stability and inhibiting cancer.
- Emerging evidence highlights p53's role in cellular and tissue homeostasis, including non-cell-autonomous functions.
- Chronic inflammation is a known promoter of cancer, and p53 actively responds to prevent neoplastic progression.
Purpose of the Study:
- To explore the multifaceted role of p53 in managing chronic inflammation and its link to cancer.
- To elucidate the complex interactions between the p53 pathway and inflammatory signaling.
- To understand how p53 status, isoforms, and mutants affect inflammatory responses and cancer development.
Main Methods:
- Review of recent literature on p53 interactions with inflammatory mediators.
- Analysis of p53's role in cellular and tissue homeostasis.
- Examination of p53's cross-talk with inflammatory pathways like NF-kappaB.
Main Results:
- p53 actively counters chronic inflammation to prevent cancer.
- p53 interacts with reactive oxygen/nitrogen species, cytokines, and immune pathways.
- p53 status, isoforms, and mutants critically determine responses, potentially promoting inflammation and cancer.
Conclusions:
- p53 plays a complex role in regulating inflammation and cancer, extending beyond its canonical tumor suppressor functions.
- The p53 pathway's interaction with inflammation is highly context-dependent on p53's molecular state.
- Dysregulation of p53 in cancer can lead to promotion of inflammation and tumorigenesis across multiple cellular compartments.
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