ArticleScientific reports2015
The energy blockers bromopyruvate and lonidamine lead GL15 glioblastoma cells to death by different p53-dependent routes.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Bypassing Blood-Brain Barrier and Glucose Dependency of Anti-Glioblastoma Drug Candidates Targeting Mitochondrial Respiration.Journal of cellular physiology · 2025Article
- Article
- Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells.Metabolites · 2024Review
- Mass spectrometry imaging discriminates glioblastoma tumor cell subpopulations and different microvascular formations based on their lipid profiles.Scientific reports · 2022Article
- Review
- Power of two: combination of therapeutic approaches involving glucose transporter (GLUT) inhibitors to combat cancer.Biochimica et biophysica acta. Reviews on cancer · 2020Review
- Article
- The Potential of Lonidamine in Combination with Chemotherapy and Physical Therapy in Cancer Treatment.Cancers · 2020Review
- Receptor tyrosine kinase targeting in glioblastoma: performance, limitations and future approaches.Contemporary oncology (Poznan, Poland) · 2020Review
- Diverse Stakeholders of Tumor Metabolism: An Appraisal of the Emerging Approach of Multifaceted Metabolic Targeting by 3-Bromopyruvate.Frontiers in pharmacology · 2019Review
- p53 and metabolism: from mechanism to therapeutics.Oncotarget · 2018Review
- Drug repurposing for the treatment of glioblastoma multiforme.Journal of experimental & clinical cancer research : CR · 2017Review
- Bitterness in sugar: O-GlcNAcylation aggravates pre-B acute lymphocytic leukemia through glycolysis via the PI3K/Akt/c-Myc pathway.American journal of cancer research · 2017Article
- The anticancer agent 3-bromopyruvate: a simple but powerful molecule taken from the lab to the bedside.Journal of bioenergetics and biomembranes · 2016Review
- Novel drugs that target the metabolic reprogramming in renal cell cancer.Cancer & metabolism · 2016Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The energy metabolism of tumor cells relies on aerobic glycolysis rather than mitochondrial oxidation. This difference between normal and cancer cells provides a biochemical basis for new therapeutic strategies aimed to block the energy power plants of cells. The effects produced by the energy blockers bromopyruvate (3BP) and lonidamine (LND) and the underlying biochemical mechanisms were investigated in GL15 glioblastoma cells. 3BP exerts early effects compared to LND, even though both drugs lead cells to death but by different routes. A dramatic decrease of ATP levels occurred after 1 hour treatment with 3BP, followed by cytochrome c and hexokinase II degradation, and by the decrease of both LC3I/LC3II ratio and p62, markers of an autophagic flux. In addition, Akt(Ser(473)) and p53(Ser(15)/Ser(315)) dephosphorylation occurred. In LND treatment, sustained ATP cellular levels were maintained up to 40 hours. The autophagic response of cells was overcome by apoptosis that was preceded by phosphatidylinositol disappearance and pAkt decrease. This last event favored p53 translocation to mitochondria triggering a p53-dependent apoptotic route, as observed at 48 and 72 hours. Adversely, in 3BP treatment, phospho-p53 dephosphorylation targeted p53 to MDM2-dependent proteolysis, thus channeling cells to irreversible autophagy.
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