ArticleThe Journal of biological chemistry2010
Characterization of functional domains necessary for mutant p53 gain of function.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
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- Targeting MCM10 disrupts cancer stemness and counteracts sorafenib resistance in hepatocellular carcinoma.Cancer gene therapy · 2025Article
- The multifunctional proline-rich domain of p53 tumor suppressor.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Knockdown of TFAP2E results in rapid GOncology letters · 2024Article
- Osteosarcoma patient with Li-Fraumeni syndrome: the first case report in Vietnam.Frontiers in oncology · 2024Article
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- Gain-of-function mutant p53: history and speculation.Journal of molecular cell biology · 2019Review
- Mutant p53 Sequestration of the MDM2 Acidic Domain Inhibits E3 Ligase Activity.Molecular and cellular biology · 2019Article
- Transcriptional Regulation by Wild-Type and Cancer-Related Mutant Forms of p53.Cold Spring Harbor perspectives in medicine · 2017Review
- TP53 Mutations in Head and Neck Squamous Cell Carcinoma and Their Impact on Disease Progression and Treatment Response.Journal of cellular biochemistry · 2016Review
- Mutant p53 and ETS2, a Tale of Reciprocity.Frontiers in oncology · 2016Review
- Mutant p53: One, No One, and One Hundred Thousand.Frontiers in oncology · 2015Review
- Mutant p53 in cancer: new functions and therapeutic opportunities.Cancer cell · 2014Review
- p53 promotes repair of heterochromatin DNA by regulating JMJD2b and SUV39H1 expression.Oncogene · 2014Article
- The consequence of oncomorphic TP53 mutations in ovarian cancer.International journal of molecular sciences · 2013Review
- Histone deacetylase inhibitors suppress mutant p53 transcription via histone deacetylase 8.Oncogene · 2013Article
- p73 expression is regulated by RNPC1, a target of the p53 family, via mRNA stability.Molecular and cellular biology · 2012Article
- Mutant p53: one name, many proteins.Genes & development · 2012Review
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tumor cells, including SW480 carcinoma cells that carry a mutant p53, are addicted to the mutant for their survival and resistance to growth suppression by chemotherapeutic agents. Here, we investigated whether various classes of p53 mutants share a common property and functional domains necessary for mutant p53 gain of function. To test this, we generated SW480 cell lines in which endogenous mutant R273H/P309S can be inducibly or stably knocked down, whereas a small interfering RNA-resistant mutant p53 along with a mutated functional domain can be inducibly or stably expressed. We found that both contact-site (R248W and R273H) and conformation (G245S and R249S) mutants are able to maintain the transformed phenotypes of SW480 cells conferred by endogenous mutant p53. We also found that activation domains 1-2 and the proline-rich domain are required for mutant p53 gain of function. Interestingly, we showed that the C-terminal basic domain, which is required for wild-type p53 activity, is an inhibitory domain for mutant p53. Furthermore, we showed that deletion of the basic domain enhances, whereas a mutation in activation domains 1-2 and deletion of the proline-rich domain abolish mutant p53 to regulate Gro1 and Id2, both of which are regulated by and mediate endogenous mutant p53 gain of function. These results indicate that both conformation and contact-site mutants share a property for cell transformation, and the domains critical for wild-type p53 tumor suppression are also required for mutant p53 tumor promotion. Thus, the inhibitory basic domain and the common property for p53 mutants can be explored for targeting tumors with mutant p53.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.