ArticleCell death & disease2023
ATAD2 is a driver and a therapeutic target in ovarian cancer that functions by upregulating CENPE.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Protein modification systems as cancer biomarkers and therapeutic targets.Precision clinical medicine · 2026Review
- Deposition of CENP-ACse4 is enhanced by mutations in the AAA+ ATPase domain of ATAD2Yta7.Genetics · 2026Article
- Bromodomain-Driven Regulation of Stem Cells: A Potential Target for Cancer Therapeutic Intervention.Stem cell reviews and reports · 2026Review
- ATAD2 drives immunotherapy resistance by promoting lactic acid-mediated CD8Frontiers in immunology · 2026Article
- ATAD2 drives melanoma growth and progression and inhibits ferroptosis.EMBO reports · 2026Article
- ATAD2 as a Cancer Target: Insights into Its Structure, Functions, Mechanisms, and Drug Development.Cancers · 2025Review
- Nodal Spread Prediction in Human Oral Tongue Squamous Cell Carcinoma Using a Cancer-Testis Antigen Genes Signature.International journal of molecular sciences · 2025Article
- Kinesin superfamily proteins in ovarian cancer: from molecular mechanisms to clinical applications.Medical oncology (Northwood, London, England) · 2025Review
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- ATAD2 Drives Prostate Cancer Progression to Metastasis.Molecular cancer research : MCR · 2025Article
- Abo1 ATPase facilitates the dissociation of FACT from chromatin.Nucleic acids research · 2025Article
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Ovarian cancer is a complex disease associated with multiple genetic and epigenetic alterations. The emergence of treatment resistance in most patients causes ovarian cancer to become incurable, and novel therapies remain necessary. We identified epigenetic regulator ATPase family AAA domain-containing 2 (ATAD2) is overexpressed in ovarian cancer and is associated with increased incidences of metastasis and recurrence. Genetic knockdown of ATAD2 or its pharmacological inhibition via ATAD2 inhibitor BAY-850 suppressed ovarian cancer growth and metastasis in both in vitro and in vivo models. Transcriptome-wide mRNA expression profiling of ovarian cancer cells treated with BAY-850 revealed that ATAD2 inhibition predominantly alters the expression of centromere regulatory genes, particularly centromere protein E (CENPE). In ovarian cancer cells, changes in CENPE expression following ATAD2 inhibition resulted in cell-cycle arrest and apoptosis induction, which led to the suppression of ovarian cancer growth. Pharmacological CENPE inhibition phenotypically recapitulated the cellular changes induced by ATAD2 inhibition, and combined pharmacological inhibition of both ATAD2 and CENPE inhibited ovarian cancer cell growth more potently than inhibition of either alone. Thus, our study identified ATAD2 as regulators of ovarian cancer growth and metastasis that can be targeted either alone or in combination with CENPE inhibitors for effective ovarian cancer therapy.
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