ArticleJournal of gynecologic oncology2019
Olaparib induced senescence under P16 or P53 dependent manner in ovarian cancer.
Article in Journal of gynecologic oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 33 citations in OpenAlex.
- Neoadjuvant PARP inhibitor scheduling in BRCA1 and BRCA2 related breast cancer: PARTNER, a randomized phase II/III trial.Nature communications · 2025Trial
- The Bidirectional Role of Cellular Senescence in the Treatment of Ovarian Cancer.Biomedicines · 2026Review
- PARP inhibitors induce a senescence phenotype in non-small cell lung carcinoma cell lines.FEBS open bio · 2026Article
- The PARP inhibitor olaparib promotes senescence in murine macrophages.GeroScience · 2026Article
- Mitochondrial priming and response to BH3 mimetics in "one-two punch" senogenic-senolytic strategies.Cell death discovery · 2025Article
- Molecular Biomarkers in Borderline Ovarian Tumors: Towards Personalized Treatment and Prognostic Assessment.Cancers · 2025Review
- TRIM4 modulates the ubiquitin-mediated degradation of hnRNPDL and weakens sensitivity to CDK4/6 inhibitor in ovarian cancer.Frontiers of medicine · 2025Article
- Eosinophilic Cells in Ovarian Borderline Serous Tumors as a Predictor of BRAF Mutation.Cancers · 2024Article
- Bcl-2 family inhibitors sensitize human cancer models to therapy.Cell death & disease · 2023Article
- Olaparib-ResistantCells · 2023Article
- Auranofin Synergizes with the PARP Inhibitor Olaparib to Induce ROS-Mediated Cell Death in Mutant p53 Cancers.Antioxidants (Basel, Switzerland) · 2023Article
- E2F1 inhibits cellular senescence and promotes oxaliplatin resistance in colorectal cancer.Annals of translational medicine · 2023Article
- Targeting Mitochondria to Control Ageing and Senescence.Pharmaceutics · 2023Review
- Targeting senescence as an anticancer therapy.Molecular oncology · 2022Review
- Development of Olaparib-Resistance Prostate Cancer Cell Lines to Identify Mechanisms Associated with Acquired Resistance.Cancers · 2022Article
- The functional multipotency of transforming growth factor β signaling at the intersection of senescence and cancer.Cellular and molecular life sciences : CMLS · 2022Review
- The protective effects of Agomelatine against Aβ1-42 oligomers-induced cellular senescence mediated by SIRT6 and Agomelatine's potential in AD treatment.Human cell · 2021Article
- Metformin Affects Olaparib Sensitivity through Induction of Apoptosis in Epithelial Ovarian Cancer Cell Lines.International journal of molecular sciences · 2021Article
- Review
- Skeletal Aging and Osteoporosis: Mechanisms and Therapeutics.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
objectivePoly (ADP-ribose) polymerase (PARP) is an important molecule in the early stress response of DNA damage, which is involved in DNA damage repair and cellular senescence. Olaparib, as PARP inhibitor, has an anti-tumor effect on high grade serous ovarian cancer, but its effects on cellular senescence have not been reported. This study intends to explore the role of olaparib in the regulation of senescence in ovarian cancer cells.
methodsThe effects of olaparib on the senescence of ovarian cancer cells were detected by using the senescence-associated β-galactosidase (SA-β-Gal) and senescence-associated heterochromatin aggregation (SAHF). Quantitative real-time polymerase chain reaction was used to analyze the senescence-associated secretory phenotype (SASP). Cell cycle and apoptosis were detected by flow cytometry. The effect of olaparib on tumor growth was analyzed in a nude mouse xenograft transplantation model.
resultsLong-term (6 days) treatment with olaparib (5 μ) significantly inhibited the growth of ovarian cancer cells, leading to arrest the cell cycle at G0/G1 phase, significant increase the number of positive SA-β-Gal stained cells and positive SAHF cells. The expression of P16 and retinoblastoma protein (p-RB) were significantly enhanced in SKOV3 cells under olaparib treated, meanwhile, the expression of P53 and p-RB were upregulated in A2780 cells. In OVCAR-3 cells, the expression of P53 was downregulated and p-RB was upregulated. Mice with SKOV3 xenograft transplantation was given olaparib (10 mg/kg/day) via abdominal cavity administration, the tumor volume was reduced (p<0.01).
conclusionContinuous low dosage administration of olaparib induced senescence under P16 or P53 dependent manner in ovarian cancer.
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