ArticleJournal of ovarian research2016
Antagonism of Bcl-XL is necessary for synergy between carboplatin and BH3 mimetics in ovarian cancer cells.
Article in Journal of ovarian research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Functional profiling of ovarian cancer models reveals Bcl-xL/NOTCH targeting to overcome resistance.NPJ precision oncology · 2026Article
- Tilting the balance of life and death: navigating DNA replication stress in cancer therapy.Experimental & molecular medicine · 2026Review
- Cell-intrinsic and tumor microenvironmental determinants of platinum resistance in epithelial ovarian cancer.Discover oncology · 2026Review
- Construction of PANoptosis-related LncRNA Prognostic Signature and Functional Analysis of AC034229.4 in Hepatocellular Carcinoma.Current medicinal chemistry · 2026Article
- Paclitaxel-induced mitotic arrest results in a convergence of apoptotic dependencies that can be safely exploited by BCL-XbioRxiv : the preprint server for biology · 2025Article
- Promising new drugs and therapeutic approaches for treatment of ovarian cancer-targeting the hallmarks of cancer.BMC medicine · 2025Review
- Pioneering the Battle Against Breast Cancer: The Promise of New Bcl-2 Family.Anti-cancer agents in medicinal chemistry · 2025Review
- Review
- Article
- Endogenous and imposed determinants of apoptotic vulnerabilities in cancer.Trends in cancer · 2023Review
- Targeting the Intrinsic Apoptosis Pathway: A Window of Opportunity for Prostate Cancer.Cancers · 2021Review
- Bcl‑2 family: Novel insight into individualized therapy for ovarian cancer (Review).International journal of molecular medicine · 2020Review
- Targeting apoptosis in cancer therapy.Nature reviews. Clinical oncology · 2020Review
- B-cell lymphoma 2 family genes show a molecular pattern of spatiotemporal heterogeneity in gynaecologic and breast cancer.Cell proliferation · 2020Article
- Pooled Genomic Screens Identify Anti-apoptotic Genes as Targetable Mediators of Chemotherapy Resistance in Ovarian Cancer.Molecular cancer research : MCR · 2019Article
- p53-Bad: A Novel Tumor Suppressor/Proapoptotic Factor Hybrid Directed to the Mitochondria for Ovarian Cancer Gene Therapy.Molecular pharmaceutics · 2019Article
- Screening a library of approved drugs reveals that prednisolone synergizes with pitavastatin to induce ovarian cancer cell death.Scientific reports · 2019Article
- ABT-737 and pictilisib synergistically enhance pitavastatin-induced apoptosis in ovarian cancer cells.Oncology letters · 2018Article
- Systems modeling accurately predicts responses to genotoxic agents and their synergism with BCL-2 inhibitors in triple negative breast cancer cells.Cell death & disease · 2018Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBH3 mimetics are a class of drugs that antagonize the Bcl-2 family of apoptosis inhibitors. We have previously shown that these compounds can potentiate the activity of carboplatin against several ovarian cancer cell lines. However, recent clinical studies have highlighted that BH3 mimetics which antagonise Bcl-XL are associated with significant thrombocytopenia. This has led to the development of ABT-199 which specifically inhibits Bcl-2. Unfortunately, Bcl-XL appears to be more frequently deregulated in ovarian cancer than Bcl-2. We therefore compared the ability of ABT-199, and the Bcl-XL selective compound WEHI-539, to potentiate the activity of carboplatin in ovarian cancer cell lines.
methodsWEHI-539, ABT-737 and ABT-199 were tested in combination with carboplatin using a panel of 6 ovarian cancer cell lines. The activity of the drugs was evaluated using cell growth assays, staining with trypan bue and measurement of apoptosis by measuring caspase 3/7 activity, PARP cleavage and annexin-V/propidium iodide staining.
resultsWe found that WEHI-539 and ABT-737, but not ABT-199, were synergistic with carboplatin in cell growth assays and potentiated cell death when assessed by trypan blue staining. Furthermore, WEHI-539 and ABT-737 augmented carboplatin induced caspase 3/7 activity, PARP cleavage and annexin V labelling, but ABT-199 failed to do so.
conclusionsThese observations suggest that compounds which target Bcl-XL are necessary if BH3 mimetics are to be successfully used to treat patients with ovarian cancer and this highlights the need to develop strategies to minimize thrombocytopenia induced by such compounds.
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