ArticleCell death and differentiation2014
Targeting proapoptotic protein BAD inhibits survival and self-renewal of cancer stem cells.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- Combining Mitomycin C with inhibition of BAD phosphorylation enhances apoptotic cell death in advanced cervical cancer.Translational oncology · 2024Article
- Cancer stem cells: advances in the glucose, lipid and amino acid metabolism.Molecular and cellular biochemistry · 2024Review
- Digital spatial profiling identifies the tumor center as a topological niche in prostate cancer characterized by an upregulation of BAD.Scientific reports · 2024Article
- MicroRNA miR-20a-5p targets CYCS to inhibit apoptosis in hepatocellular carcinoma.Cell death & disease · 2024Article
- AMPK inhibition sensitizes acute leukemia cells to BH3 mimetic-induced cell death.Cell death and differentiation · 2024Article
- Luteolin enhances erlotinib's cell proliferation inhibitory and apoptotic effects in glioblastoma cell lines.Frontiers in pharmacology · 2022Article
- Emerging role of BAD and DAD1 as potential targets and biomarkers in cancer.Oncology letters · 2021Review
- Review
- Transcriptome Profiling of mInternational journal of molecular sciences · 2021Article
- Article
- Profile of Basal Cell Carcinoma Mutations and Copy Number Alterations - Focus on Gene-Associated Noncoding Variants.Frontiers in oncology · 2021Article
- Pharmacological Inhibition of BAD Ser99 Phosphorylation Enhances the Efficacy of Cisplatin in Ovarian Cancer by Inhibition of Cancer Stem Cell-like Behavior.ACS pharmacology & translational science · 2020Article
- BAD inactivation exacerbates rheumatoid arthritis pathology by promoting survival of sublining macrophages.eLife · 2020Article
- Arctigenin Attenuates Breast Cancer Progression through Decreasing GM-CSF/TSLP/STAT3/β-Catenin Signaling.International journal of molecular sciences · 2020Article
- Dual-targeted therapeutic strategy combining CSC-DC-based vaccine and cisplatin overcomes chemo-resistance in experimental mice model.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- B-cell lymphoma 2 family genes show a molecular pattern of spatiotemporal heterogeneity in gynaecologic and breast cancer.Cell proliferation · 2020Article
- Differential responsiveness to BRAF inhibitors of melanoma cell lines BRAF V600E-mutated.Journal of translational medicine · 2020Article
- GPER-induced signaling is essential for the survival of breast cancer stem cells.International journal of cancer · 2020Article
- Targeting cancer stem cells from a metabolic perspective.Experimental biology and medicine (Maywood, N.J.) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
Emerging evidence suggests that the resistance of cancer stem cells (CSC) to many conventional therapies is one of the major limiting factors of cancer therapy efficacy. Identification of mechanisms responsible for survival and self-renewal of CSC will help design new therapeutic strategies that target and eliminate both differentiated cancer cells and CSC. Here we demonstrated the potential role of proapoptotic protein BAD in the biology of CSC in melanoma, prostate and breast cancers. We enriched CD44(+)/CD24(-) cells (CSC) by tumorosphere formation and purified this population by FACS. Both spheres and CSC exhibited increased potential for proliferation, migration, invasion, sphere formation, anchorage-independent growth, as well as upregulation of several stem cell-associated markers. We showed that the phosphorylation of BAD is essential for the survival of CSC. Conversely, ectopic expression of a phosphorylation-deficient mutant BAD induced apoptosis in CSC. This effect was enhanced by treatment with a BH3-mimetic, ABT-737. Both pharmacological agents that inhibit survival kinases and growth factors that are involved in drug resistance delivered their respective cytotoxic and protective effects by modulating the BAD phosphorylation in CSC. Furthermore, the frequency and self-renewal capacity of CSC was significantly reduced by knocking down the BAD expression. Consistent with our in vitro results, significant phosphorylation of BAD was found in CD44(+) CSC of 83% breast tumor specimens. In addition, we also identified a positive correlation between BAD expression and disease stage in prostate cancer, suggesting a role of BAD in tumor advancement. Our studies unveil the role of BAD in the survival and self-renewal of CSC and propose BAD not only as an attractive target for cancer therapy but also as a marker of tumor progression.
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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.