ArticleCell cycle (Georgetown, Tex.)2014
Distinctive effects of the cellular inhibitor of apoptosis protein c-IAP2 through stabilization by XIAP in glioblastoma multiforme cells.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- BIRC3 and BIRC5: multi-faceted inhibitors in cancer.Cell & bioscience · 2021Review
- A small-molecule ARTS mimetic promotes apoptosis through degradation of both XIAP and Bcl-2.Cell death & disease · 2020Article
- Anti-apoptotic proteins in the autophagic world: an update on functions of XIAP, Survivin, and BRUCE.Journal of biomedical science · 2020Review
- Targeting the Ubiquitin System in Glioblastoma.Frontiers in oncology · 2020Review
- Sustained NF-κB-STAT3 signaling promotes resistance to Smac mimetics in Glioma stem-like cells but creates a vulnerability to EZH2 inhibition.Cell death discovery · 2019Article
- Immunohistochemical Characterization of Procaspase-3 Overexpression as a Druggable Target With PAC-1, a Procaspase-3 Activator, in Canine and Human Brain Cancers.Frontiers in oncology · 2019Article
- Combination of quercetin and cisplatin enhances apoptosis in OSCC cells by downregulating xIAP through the NF-κB pathway.Journal of Cancer · 2019Article
- Drug Repositioning in Glioblastoma: A Pathway Perspective.Frontiers in pharmacology · 2018Review
- Analysis of the inhibitors of apoptosis identifies BIRC3 as a facilitator of malignant progression in glioma.Oncotarget · 2017Article
- Apoptotic Signaling Pathways in Glioblastoma and Therapeutic Implications.BioMed research international · 2017Review
- The 1,4 benzoquinone-featured 5-lipoxygenase inhibitor RF-Id induces apoptotic death through downregulation of IAPs in human glioblastoma cells.Journal of experimental & clinical cancer research : CR · 2016Article
- Transcriptome sequencing of neurologic diseases associated genes in HHV-6A infected human astrocyte.Oncotarget · 2016Article
- BIRC3 is a novel driver of therapeutic resistance in Glioblastoma.Scientific reports · 2016Article
- Review
- Article
- Enhanced glioblastoma immunotherapy via SMAC mimetic dose escalation and TGFβ blockade.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Inhibitor of apoptosis proteins (IAPs) are extensively involved in NFκB signaling pathways. Regulation of c-IAP2 turnover by other proteins was investigated in glioblastoma multiforme (GBM) cells in the present study. When overexpressed, X-linked IAP (XIAP) enhanced expression of ectopic c-IAP2, but not c-IAP1, and endogenous c-IAP2 levels were reduced once XIAP expression was silenced. TNFα stimulation substantially increased c-IAP2 expression, and this upregulation was impaired by suppression of XIAP. Similarly, when XIAP was limiting due to severe hypoxic conditions, c-IAP2 levels were downregulated. These data together indicate that XIAP is an important regulator responsible for stabilization of c-IAP2 levels under different conditions. Protein interactions occur through binding of BIR2 and BIR3 domains of c-IAP2 with the RING finger of XIAP. XIAP inhibition of c-IAP2 auto-degradation was dependent on this physical interaction, and it was independent of XIAP E3 ligase activity. Global c-IAP2 ubiquitination was not affected by XIAP, although c-IAP2 levels were significantly increased. A CARD-RING-containing fragment of c-IAP2 was found to target XIAP for proteasome-independent degradation, but it was unable to sensitize GBM cells to chemo-reagents. The XIAP-stabilized c-IAP2 was found to enhance IκB-α phosphorylation on serines 32 and 36, and to antagonize XIAP-induced increase in mature Smac and Bcl10. Taken together, our data identify a distinctive role of c-IAP2 as stabilizer of XIAP, which is likely involved in regulation of NFκB activation and apoptosis in GBM cells.
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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.