ArticleCancer research2016
Mutant p53 Promotes Epithelial Ovarian Cancer by Regulating Tumor Differentiation, Metastasis, and Responsiveness to Steroid Hormones.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- The Role of Neutrophil Extracellular Traps (NETs) in the Pathogenesis of Ovarian Cancer: New Insight and Future Perspectives.Molecular biotechnology · 2026Review
- Cellular origins of mucinous ovarian carcinoma.The Journal of pathology · 2025Review
- Gold Nanoprobes for Robust Colorimetric Detection of Nucleic Acid Sequences Related to Disease Diagnostics.Nanomaterials (Basel, Switzerland) · 2024Review
- Regulation of ULK1 by WTAP/IGF2BP3 axis enhances mitophagy and progression in epithelial ovarian cancer.Cell death & disease · 2024Article
- Biology-driven therapy advances in high-grade serous ovarian cancer.The Journal of clinical investigation · 2024Review
- Progress in Anticancer Drug Development Targeting Ubiquitination-Related Factors.International journal of molecular sciences · 2022Review
- Harnessing preclinical models for the interrogation of ovarian cancer.Journal of experimental & clinical cancer research : CR · 2022Review
- The senescence-associated secretory phenotype in ovarian cancer dissemination.American journal of physiology. Cell physiology · 2022Review
- Preclinical models of epithelial ovarian cancer: practical considerations and challenges for a meaningful application.Cellular and molecular life sciences : CMLS · 2022Review
- Ubiquitin ligase DTX3 empowers mutant p53 to promote ovarian cancer development.Genes & diseases · 2022Article
- Article
- Deciphering the Increased Prevalence of TP53 Mutations in Metastatic Prostate Cancer.Cancer informatics · 2022Article
- Aberrant MAPK Signaling Offers Therapeutic Potential for Treatment of Ovarian Carcinoma.OncoTargets and therapy · 2022Review
- Identification ofOncology letters · 2021Article
- Polyploid giant cancer cells and ovarian cancer: new insights into mitotic regulators and polyploidy†.Biology of reproduction · 2021Review
- BCL7C suppresses ovarian cancer growth by inactivating mutant p53.Journal of molecular cell biology · 2021Article
- Cellular models of development of ovarian high-grade serous carcinoma: A review of cell of origin and mechanisms of carcinogenesis.Cell proliferation · 2021Review
- Murine Cytomegalovirus M25 Proteins Sequester the Tumor Suppressor Protein p53 in Nuclear Accumulations.Journal of virology · 2020Article
- The hallmarks of ovarian cancer: proliferation and cell growth.EJC supplements : EJC : official journal of EORTC, European Organization for Research and Treatment of Cancer ... [et al.] · 2020Article
- Modelling Epithelial Ovarian Cancer in Mice: Classical and Emerging Approaches.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the tumor protein p53 (TP53) are the most frequently occurring genetic events in high-grade ovarian cancers, especially the prevalence of the Trp53(R172H)-mutant allele. In this study, we investigated the impact of the Trp53(R172H)-mutant allele on epithelial ovarian cancer (EOC) in vivo We used the Pten/Kras(G12D)-mutant mouse strain that develops serous EOC with 100% penetrance to introduce the mutant Trp53(R172H) allele (homolog for human Trp53(R172H)). We demonstrate that the Trp53(R172H) mutation promoted EOC but had differential effects on disease features and progression depending on the presence or absence of the wild-type (WT) TP53 allele. Heterozygous WT/Trp53(R172H) alleles facilitated invasion into the ovarian stroma, accelerated intraperitoneal metastasis, and reduced TP53 transactivation activity but retained responsiveness to nutlin-3a, an activator of WT TP53. Moreover, high levels of estrogen receptor α in these tumors enhanced the growth of both primary and metastatic tumors in response to estradiol. Ovarian tumors homozygous for Trp53(R172H) mutation were undifferentiated and highly metastatic, exhibited minimal TP53 transactivation activity, and expressed genes with potential regulatory functions in EOC development. Notably, heterozygous WT/Trp53(R172H) mice also presented mucinous cystadenocarcinomas at 12 weeks of age, recapitulating human mucinous ovarian tumors, which also exhibit heterozygous TP53 mutations (∼50%-60%) and KRAS mutations. Therefore, we present the first mouse model of mucinous tumor formation from ovarian cells and supporting evidence that mutant TP53 is a key regulator of EOC progression, differentiation, and responsiveness to steroid hormones. Cancer Res; 76(8); 2206-18. ©2016 AACR.
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