ArticleCancers2020
Venetoclax, a BCL-2 Inhibitor, Enhances the Efficacy of Chemotherapeutic Agents in Wild-Type ABCG2-Overexpression-Mediated MDR Cancer Cells.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- PIM1-mediated signalling as a therapeutic target in breast cancer: repurposing venetoclax for targeted inhibition.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Moracin D Inhibits Gastric Cancer Progression Through B-Cell Lymphoma-2 (Bcl-2)-Mediated Cell Cycle Arrest and Apoptosis, Enhancing Chemotherapy Efficacy.Biomolecules · 2026Article
- B-9-8, a Novel Harman Dimer, Reverses ABCG2-mediated Chemotherapeutic Drug Resistance.Recent patents on anti-cancer drug discovery · 2026Article
- Talazoparib and radiation enhance the senolytic efficacy of venetoclax in therapy-induced senescent triple-negative breast cancer cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025Article
- Synthesis of novel pyridazine and pyrimidine linked pyrazole derivatives as DNA ligase 1 and IV inhibitors that induce apoptosis.Chemico-biological interactions · 2025Article
- Gold complex QB1561 suppresses drug-resistant cancer cells by inhibiting TrxR and mitochondrial respiratory function.Frontiers in pharmacology · 2025Article
- Reversal of ABCG2-mediated drug resistance by tinodasertib (ETC-206).Frontiers in pharmacology · 2025Article
- Cellular and molecular aspects of drug resistance in cancers.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024Review
- ATP-Binding Cassette Subfamily G Member 2 in Acute Myeloid Leukemia: A New Molecular Target?Biomedicines · 2024Review
- Integrative genomic analyses combined with molecular dynamics simulations reveal the impact of deleterious mutations of Bcl-2 gene on the apoptotic machinery and implications in carcinogenesis.Frontiers in genetics · 2024Article
- ABCC1 and glutathione metabolism limit the efficacy of BCL-2 inhibitors in acute myeloid leukemia.Nature communications · 2023Article
- Article
- ABCG2 in Acute Myeloid Leukemia: Old and New Perspectives.International journal of molecular sciences · 2023Review
- The AKT inhibitor, MK-2206, attenuates ABCG2-mediated drug resistance in lung and colon cancer cells.Frontiers in pharmacology · 2023Article
- MET inhibitor tepotinib antagonizes multidrug resistance mediated by ABCG2 transporter:Acta pharmaceutica Sinica. B · 2022Article
- Multidrug Resistance (MDR): A Widespread Phenomenon in Pharmacological Therapies.Molecules (Basel, Switzerland) · 2022Review
- Sorafenib, rapamycin, and venetoclax attenuate doxorubicin-induced senescence and promote apoptosis in HCT116 cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022Article
- Review
- Article
- The Novel Benzamide Derivative, VKNG-2, Restores the Efficacy of Chemotherapeutic Drugs in Colon Cancer Cell Lines by Inhibiting the ABCG2 Transporter.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Previous studies have shown that small-molecule BCL-2 inhibitors can have a synergistic interaction with ABCG2 substrates in chemotherapy. Venetoclax is a potent and selective BCL-2 inhibitor, approved by the FDA in 2016 for the treatment of patients with chronic lymphocytic leukemia (CLL). This study showed that, at a non-toxic concentration, venetoclax at 10 µM significantly reversed multidrug resistance (MDR) mediated by wild-type ABCG2, without significantly affecting MDR mediated by mutated ABCG2 (R482G and R482T) and ABCB1, while moderate or no reversal effects were observed at lower concentrations (0.5 to 1 µM). The results showed that venetoclax increased the intracellular accumulation of chemotherapeutic agents, which was the result of directly blocking the wild-type ABCG2 efflux function and inhibiting the ATPase activity of ABCG2. Our study demonstrated that venetoclax potentiates the efficacy of wild-type ABCG2 substrate drugs. These findings may provide useful guidance in combination therapy against wild-type ABCG2-mediated MDR cancer in clinical practice.
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Registered trials
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.