ArticleNeoplasia (New York, N.Y.)2008
BH3 mimetics reactivate autophagic cell death in anoxia-resistant malignant glioma cells.
Article in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Autophagy in cancers including brain tumors: role of MicroRNAs.Cell communication and signaling : CCS · 2020Review
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- Isocitrate dehydrogenase 1 and 2 mutations induce BCL-2 dependence in acute myeloid leukemia.Nature medicine · 2015Article
- Interrogation of gossypol therapy in glioblastoma implementing cell line and patient-derived tumour models.British journal of cancer · 2014Article
- Understanding sensitivity to BH3 mimetics: ABT-737 as a case study to foresee the complexities of personalized medicine.Journal of molecular signaling · 2012Article
- Autophagy in brain tumors: a new target for therapeutic intervention.Brain pathology (Zurich, Switzerland) · 2012Review
- Distinct cellular and therapeutic effects of obatoclax in rituximab-sensitive and -resistant lymphomas.British journal of haematology · 2011Article
- Characterization of Puma-dependent and Puma-independent neuronal cell death pathways following prolonged proteasomal inhibition.Molecular and cellular biology · 2010Article
- Dinosaurs and ancient civilizations: reflections on the treatment of cancer.Neoplasia (New York, N.Y.) · 2010Article
- The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009Article
- Synthetic galectin-3 inhibitor increases metastatic cancer cell sensitivity to taxol-induced apoptosis in vitro and in vivo.Neoplasia (New York, N.Y.) · 2009Article
- Neoplasia: the second decade.Neoplasia (New York, N.Y.) · 2008Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here, we investigated the specific roles of Bcl-2 family members in anoxia tolerance of malignant glioma. Flow cytometry analysis of cell death in 17 glioma cell lines revealed drastic differences in their sensitivity to oxygen withdrawal (<0.1% O(2)). Cell death correlated with mitochondrial depolarization, cytochrome C release, and translocation of green fluorescent protein (GFP)-tagged light chain 3 to autophagosomes but occurred in the absence of caspase activation or phosphatidylserine exposure. In both sensitive and tolerant glioma cell lines, anoxia caused a significant up-regulation of BH3-only genes previously implicated in mediating anoxic cell death in other cell types (BNIP3, NIX, PUMA, and Noxa). In contrast, we detected a strong correlation between anoxia resistance and high expression levels of antiapoptotic Bcl-2 family proteins Bcl-xL, Bcl-2, and Mcl-1 that function to neutralize the proapoptotic activity of BH3-only proteins. Importantly, inhibition of both Bcl-2 and Bcl-xL with the small-molecule BH3 mimetics HA14-1 and BH3I-2' and by RNA interference reactivated anoxia-induced autophagic cell death in previously resistant glioma cells. Our data suggest that endogenous BH3-only protein induction may not be able to compensate for the high expression of antiapoptotic Bcl-2 family proteins in anoxia-resistant astrocytomas. They also support the conjecture that BH3 mimetics may represent an exciting new approach for the treatment of malignant glioma.
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