ArticleNature communications2022
Co-targeting of BAX and BCL-XL proteins broadly overcomes resistance to apoptosis in cancer.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
100 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.
- Mechanisms of traditional Chinese medicine overcoming of radiotherapy resistance in breast cancer.Frontiers in oncology · 2024Pooled it
- RBM protein family: Focusing on the occurrence, progression and treatment of cancer.Medical oncology (Northwood, London, England) · 2026Review
- Synergistic p53 Pathway Activation Through Sono-Gene Therapy Induced by Ultrasound-Triggered Theranostic Mesoporous Nanoparticles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- 2-Pyrazoline-5-One Derivative Suppresses Cell Proliferation and Induces Apoptosis With Upregulation of Bax in Breast Cancer Cells.Journal of biochemical and molecular toxicology · 2026Article
- JAB1/CRL4B complex represses PPARG/ACSL5 expression to promote breast tumorigenesis.Cell death and differentiation · 2026Article
- Synergistic apoptotic and epithelial-mesenchymal transition-inhibitory effects ofVeterinary world · 2026Article
- Targeting the DDX3/PAF1 axis enhances chemotherapy efficacy in pancreatic ductal adenocarcinoma.Cancer letters · 2026Article
- Quinoxaline as Dual Modulators of Apoptotic Regulators Bcl-2 and Bax: A Combined In Vitro and In Silico Anticancer Approach.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Antiproliferative effect of Filopaludina bengalensis fluid inducing apoptosis-necroptosis synergy with immunogenic remodelling in triple-negative breast cancer.Scientific reports · 2025Article
- Allosteric regulation of BH3-in-groove interactions by tail anchors of BCL-xL complexes limits BH3 mimetic antagonism.Nature communications · 2025Article
- The potential of Eco-friendly synthesis of multifunctional ZnO-CuO nanocomposites using Mentha longifolia extract for their biomedical applications.Journal of materials science. Materials in medicine · 2025Article
- Genomic copy-number variants drive apoptotic evasion underlying acquired resistance to immune checkpoint inhibitors.Immunity · 2025Article
- Cancer and Aging Biomarkers: Classification, Early Detection Technologies and Emerging Research Trends.Biosensors · 2025Review
- [Combination of proteome and transcriptome analysis to predict survival and immunotherapy response in patients with head and neck squamous cell carcinoma].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025Article
- Article
- Apoptosis regulators of the Bcl-2 family play a key role in chemoresistance of cholangiocarcinoma organoids.International journal of cancer · 2025Article
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- Design, synthesis, and in vitro antitumor evaluation of novel benzimidazole acylhydrazone derivatives.Molecular diversity · 2025Article
- Unraveling the meta-hallmarks between senescent and tumor cells: A new perspective for senolytic drug discovery.Acta pharmaceutica Sinica. B · 2025Review
- Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms.Pharmacology research & perspectives · 2025Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Deregulation of the BCL-2 family interaction network ensures cancer resistance to apoptosis and is a major challenge to current treatments. Cancer cells commonly evade apoptosis through upregulation of the BCL-2 anti-apoptotic proteins; however, more resistant cancers also downregulate or inactivate pro-apoptotic proteins to suppress apoptosis. Here, we find that apoptosis resistance in a diverse panel of solid and hematological malignancies is mediated by both overexpression of BCL-XL and an unprimed apoptotic state, limiting direct and indirect activation mechanisms of pro-apoptotic BAX. Both survival mechanisms can be overcome by the combination of an orally bioavailable BAX activator, BTSA1.2 with Navitoclax. The combination demonstrates synergistic efficacy in apoptosis-resistant cancer cells, xenografts, and patient-derived tumors while sparing healthy tissues. Additionally, functional assays and genomic markers are identified to predict sensitive tumors to the combination treatment. These findings advance the understanding of apoptosis resistance mechanisms and demonstrate a novel therapeutic strategy for cancer treatment.
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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.