ArticleOncogene2016
BIRC5/Survivin as a target for glycolysis inhibition in high-stage neuroblastoma.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 93 citations in OpenAlex.
- Design of Anti-Tumor RNA Nanoparticles and Their Inhibitory Effect on Hep3B Liver Cancer.Biomolecules · 2025Article
- From bioinformatics to clinical translation: BIRC5 as a pivotal diagnostic biomarker and therapeutic target for NAFLD-driven HCC.Cell biology and toxicology · 2025Article
- Survivin can alter mitochondrial architecture by regulating phosphatidylethanolamine synthesis.Journal of cell science · 2025Article
- Targeting tumor angiogenesis and metabolism: a new perspective in pediatric thoracic tumor therapy.Frontiers in cell and developmental biology · 2025Review
- Defining neuroblastoma: From origin to precision medicine.Neuro-oncology · 2024Review
- Review
- Article
- Review
- MYCN and SNRPD3 cooperate to maintain a balance of alternative splicing events that drives neuroblastoma progression.Oncogene · 2024Article
- Article
- The survivin-ran inhibitor LLP-3 decreases oxidative phosphorylation, glycolysis and growth of neuroblastoma cells.BMC cancer · 2023Article
- Identification of Molecular Subtypes and Prognostic Characteristics of Adrenocortical Carcinoma Based on Unsupervised Clustering.International journal of molecular sciences · 2023Article
- TP53RK Drives the Progression of Chronic Kidney Disease by Phosphorylating Birc5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The Prognostic and Therapeutic Implications of the Chemoresistance Gene BIRC5 in Triple-Negative Breast Cancer.Cancers · 2022Article
- A Metabolism-Related Gene Prognostic Index for Prediction of Response to Immunotherapy in Lung Adenocarcinoma.International journal of molecular sciences · 2022Article
- [Prognosis prediction model for hepatocellular carcinoma based on autophagy related genes].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2022Article
- Analysis of Mitochondrial Function, Structure, and Intracellular Organization In Situ in Cardiomyocytes and Skeletal Muscles.International journal of molecular sciences · 2022Review
- Study on differentially expressed genes between stage M and stage MS neuroblastoma.Frontiers in oncology · 2022Article
- Schisantherin A inhibits cell proliferation by regulating glucose metabolism pathway in hepatocellular carcinoma.Frontiers in pharmacology · 2022Article
- Structural and functional remodeling of mitochondria as an adaptive response to energy deprivation.Biochimica et biophysica acta. Bioenergetics · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adverse forms of neuroblastoma (NB), a childhood malignancy that develops from immature neuronal progenitor cells frequently carry a gain of chromosome 17q, which leads to overexpression of the antiapoptotic protein BIRC5/Survivin. We have recently shown that high Survivin expression shuts down mitochondrial complex I activity and shifts NB cells from oxidative phosphorylation to aerobic glycolysis, which further increases resistance to cell death induction. This increased glucose consumption sensitized tumor cells to glycolysis inhibitors. Interestingly, in Survivin-overexpressing cells 2-deoxy-d-glucose (2DG) treatment induces re-fusion of mitochondrial networks after 4 h, which coincides with Survivin repression. 2DG selectively acts on Survivin-expressing NB cells and induces autophagic degradation of Survivin via activation of the E3-ubiquitin ligase Parkin, a downstream target of PINK1. Survivin degradation further releases bound Beclin-1, which enhances autophagy and cell death induction. Knockdown of Parkin, however, reduces the sensitivity of Survivin-expressing NB cells to glycolysis inhibition. The selective activity of 2DG treatment on Survivin-overexpressing tumor cells was also confirmed in a xenograft mouse model, which further supports our hypothesis that glycolysis inhibitors might be useful drugs in the treatment of NB.
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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.