ArticleOncogene2018
PAX8 activates a p53-p21-dependent pro-proliferative effect in high grade serous ovarian carcinoma.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
- High KPNA2 expression predicts poor prognosis in pathological T4 colorectal cancer by importing c-Myc into the nucleus to suppress p53-dependent p21 expression.British journal of cancer · 2026Article
- Article
- Alterations in mitochondria and cellular senescence in aged sEH null female kidneys.GeroScience · 2026Article
- Cancer Cell Dormancy and Chemotherapy Resistance.Journal of Cancer · 2026Review
- Silencing KMT2A with siRNA induces apoptosis and cell cycle arrest in high-grade serous ovarian carcinoma cells by modulating GOF p53-dependent pathways, highlighting its potential as a therapeutic target.Medical oncology (Northwood, London, England) · 2025Article
- Integrative multi-omic analysis reveals a PAX8-driven gene network linking tumor stemness to therapy response in ovarian cancer.NAR genomics and bioinformatics · 2025Article
- Establishment and characterization of preclinical model of primary ovarian squamous cell carcinoma.Human cell · 2025Article
- PAX Family, Master Regulator in Cancer.Diagnostics (Basel, Switzerland) · 2025Review
- Identifying key multifunctional components shared by critical cancer and normal liver pathways via SparseGMM.Cell reports methods · 2023Article
- PAX8 in the Junction between Development and Tumorigenesis.International journal of molecular sciences · 2022Review
- The transcription factor PAX8 promotes angiogenesis in ovarian cancer through interaction with SOX17.Science signaling · 2022Article
- SOX17 and PAX8 constitute an actionable lineage-survival transcriptional complex in ovarian cancer.Oncogene · 2022Article
- PAX8 as a Potential Target for Ovarian Cancer: What We Know so Far.OncoTargets and therapy · 2022Review
- ERK-mediated Cytoplasmic Retention of USP11 Contributes to Breast Cancer Cell Proliferation by Stabilizing Cytoplasmic p21.International journal of biological sciences · 2022Article
- Article
- Article
- Review
- FOXM1: A Multifunctional Oncoprotein and Emerging Therapeutic Target in Ovarian Cancer.Cancers · 2021Review
- Adipose-derived mesenchymal stem cells induced PAX8 promotes ovarian cancer cell growth by stabilizing TAZ protein.Journal of cellular and molecular medicine · 2021Article
- Chloroxine overrides DNA damage tolerance to restore platinum sensitivity in high-grade serous ovarian cancer.Cell death & disease · 2021Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High grade serous carcinoma (HGSC) is the most common subtype of ovarian cancer and it is now widely accepted that this disease often originates from the fallopian tube epithelium. PAX8 is a fallopian tube lineage marker with an essential role in embryonal female genital tract development. In the adult fallopian tube, PAX8 is expressed in the fallopian tube secretory epithelial cell (FTSEC) and its expression is maintained through the process of FTSEC transformation to HGSC. We now report that PAX8 has a pro-proliferative and anti-apoptotic role in HGSC. The tumor suppressor gene TP53 is mutated in close to 100% of HGSC; in the majority of cases, these are missense mutations that endow the mutant p53 protein with potential gain of function (GOF) oncogenic activities. We show that PAX8 positively regulates the expression of TP53 in HGSC and the pro-proliferative role of PAX8 is mediated by the GOF activity of mutant p53. Surprisingly, mutant p53 transcriptionally activates the expression of p21, which localizes to the cytoplasm of HGSC cells where it plays a non-canonical, pro-proliferative role. Together, our findings illustrate how TP53 mutations in HGSC subvert a normal regulatory pathway into a driver of tumor progression.
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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.