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Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
Deconstructing networks of p53-mediated tumor suppression in vivo
Alyssa M Kaiser1, Laura D Attardi1,2
1Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
Abstract:
The transcription factor p53 is a vital tumor suppressor. Upon activation by diverse stresses including oncogene activation, DNA damage, hypoxia and nutrient deprivation, p53 activates a panoply of target genes and orchestrates numerous downstream responses that suppress tumorigenesis. Although early studies of p53 suggested that its ability to induce cell cycle arrest, senescence and apoptosis programs accounted for its tumor-suppressor activity, more recent studies have challenged this notion. Moreover, p53 regulates a suite of additional processes, such as metabolism, stem cell function, invasion and metastasis. The processes p53 coordinately regulates to enact tumor suppression, and how such regulation occurs, thus remain elusive. In this review, we will summarize our current knowledge of p53-mediated tumor-suppressive mechanisms gleaned from in vivo studies in mouse models.
Insights
The tumor suppressor p53, activated by stress, orchestrates gene networks to prevent cancer. Its tumor-suppressive roles extend beyond cell death to include metabolism and metastasis, as revealed by mouse models.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The transcription factor p53 is a critical tumor suppressor.
- p53 is activated by various stresses like DNA damage and hypoxia.
- Its role in tumor suppression is complex and involves more than apoptosis.
Purpose of the Study:
- To review the multifaceted tumor-suppressive mechanisms of p53.
- To explore p53's regulation of genes, metabolism, and metastasis.
- To summarize findings from in vivo mouse studies on p53.
Main Methods:
- Literature review of in vivo studies in mouse models.
- Analysis of p53's target genes and downstream responses.
- Examination of p53's regulation of cellular processes.
Main Results:
- p53 activation by stress initiates gene expression programs.
- p53 influences cell cycle arrest, senescence, and apoptosis.
- p53 also regulates metabolism, stem cell function, invasion, and metastasis.
Conclusions:
- p53 employs diverse mechanisms to suppress tumors.
- Understanding these mechanisms is crucial for cancer research.
- In vivo mouse studies provide key insights into p53's function.
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