ArticleOncotarget2014
Bak and Mcl-1 are essential for Temozolomide induced cell death in human glioma.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 52 citations in OpenAlex.
- Selinexor enhances temozolomide efficacy in glioblastoma through modulation of multiple resistance-associated mechanisms.Frontiers in oncology · 2026Article
- PLD1 is a key player in cancer stemness and chemoresistance: Therapeutic targeting of cross-talk between the PI3K/Akt and Wnt/β-catenin pathways.Experimental & molecular medicine · 2024Review
- Development of an MCL-1-related prognostic signature and inhibitors screening for glioblastoma.Frontiers in pharmacology · 2023Article
- Noxa and Mcl-1 expression influence the sensitivity to BH3-mimetics that target Bcl-xL in patient-derived glioma stem cells.Scientific reports · 2022Article
- Regorafenib Reverses Temozolomide-Induced CXCL12/CXCR4 Signaling and Triggers Apoptosis Mechanism in Glioblastoma.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Cellular Heterogeneity and Cooperativity in Glioma Persister Cells Under Temozolomide Treatment.Frontiers in cell and developmental biology · 2022Article
- Cinnamophilin enhances temozolomide-induced cytotoxicity against malignant glioma: the roles of ROS and cell cycle arrest.Translational cancer research · 2021Article
- Autophagy inhibition is the next step in the treatment of glioblastoma patients following the Stupp era.Cancer gene therapy · 2021Review
- Oncolytic Virus-Induced Autophagy in Glioblastoma.Cancers · 2021Review
- Z-scan method to measure the nonlinear optical behavior of cells for evaluating the cytotoxic effects of chemotherapy and hyperthermia treatments.Lasers in medical science · 2021Article
- Phospholipase D1 inhibition sensitizes glioblastoma to temozolomide and suppresses its tumorigenicity.The Journal of pathology · 2020Article
- Sphingolipid distribution at mitochondria-associated membranes (MAMs) upon induction of apoptosis.Journal of lipid research · 2020Article
- Identification of a transient state during the acquisition of temozolomide resistance in glioblastoma.Cell death & disease · 2020Article
- Drug resistance in glioblastoma: are persisters the key to therapy?Cancer drug resistance (Alhambra, Calif.) · 2020Review
- A Potential Mechanism of Temozolomide Resistance in Glioma-Ferroptosis.Frontiers in oncology · 2020Article
- Autophagic and Apoptotic Pathways as Targets for Chemotherapy in Glioblastoma.International journal of molecular sciences · 2018Review
- Novel Targeting of Transcription and Metabolism in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Melanocortin Receptor-4 Gene Polymorphisms in Glioblastoma Patients Treated with Concomitant Radio-Chemotherapy.Molecular neurobiology · 2018Article
- [MACF1 knockdown in glioblastoma multiforme cells increases temozolomide-induced cytotoxicity].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
- Therapeutic interactions of autophagy with radiation and temozolomide in glioblastoma: evidence and issues to resolve.British journal of cancer · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temozolomide (TMZ) is an alkylating agent used for the treatment of glioblastoma multiforme (GBM), the main form of human brain tumours in adults. It has been reported that TMZ induced DNA lesions that subsequently trigger cell death but the actual mechanisms involved in the process are still unclear. We investigated the implication of major proteins of the Bcl-2 family in TMZ-induced cell death in GBM cell lines at concentrations closed to that reached in the brain during the treatments. We did not observe modulation of autophagy at these concentrations but we found an induction of apoptosis. Using RNA interference, we showed that TMZ induced apoptosis is dependent on the pro-apoptotic protein Bak but independent of the pro-apoptotic protein Bax. Apoptosis was not enhanced by ABT-737, an inhibitor of Bcl-2/Bcl-Xl/Bcl-W but not Mcl-1. The knock-down of Mcl-1 expression increased TMZ induced apoptosis. Our results identify a Mcl-1/Bak axis for TMZ induced apoptosis in GBM and thus unravel a target to overcome therapeutic resistance toward TMZ.
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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.