ArticleJournal of experimental & clinical cancer research : CR2017
Rapamycin (mTORC1 inhibitor) reduces the production of lactate and 2-hydroxyglutarate oncometabolites in IDH1 mutant fibrosarcoma cells.
Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Resistance to Targeted Therapy in AML: Current Challenges and Emerging Treatment Strategies.Journal of clinical medicine · 2026Review
- Rapamycin suppresses small bowel adenocarcinoma HUTU 80 cells proliferation by inhibiting hypoxia-inducible factor-1α mediated metabolic reprogramming.World journal of gastrointestinal oncology · 2025Article
- Microbial infection and treatment strategies in cancer patients.Frontiers in microbiology · 2025Review
- mTOR hyperactivity andPathology oncology research : POR · 2024Review
- Synthetic lethality and synergetic effect: the effective strategies for therapy of IDH-mutated cancers.Journal of experimental & clinical cancer research : CR · 2021Review
- Novel mTORC1 Inhibitors Kill Glioblastoma Stem Cells.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Inhibition of Metabolic Shift can Decrease Therapy Resistance in Human High-Grade Glioma Cells.Pathology oncology research : POR · 2020Article
- PI3K/mTOR inhibition of IDH1 mutant glioma leads to reduced 2HG production that is associated with increased survival.Scientific reports · 2019Article
- mTORC1 as a Regulator of Mitochondrial Functions and a Therapeutic Target in Cancer.Frontiers in oncology · 2019Review
- GABA, glutamine, glutamate oxidation and succinic semialdehyde dehydrogenase expression in human gliomas.Journal of experimental & clinical cancer research : CR · 2018Article
- Targeting cellular metabolism using rapamycin and/or doxycycline enhances anti-tumour effects in human glioma cells.Cancer cell international · 2018Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMultiple studies concluded that oncometabolites (e.g. D-2-hydroxyglutarate (2-HG) related to mutant isocitrate dehydrogenase 1/2 (IDH1/2) and lactate) have tumour promoting potential. Regulatory mechanisms implicated in the maintenance of oncometabolite production have great interest. mTOR (mammalian target of rapamycin) orchestrates different pathways, influences cellular growth and metabolism. Considering hyperactivation of mTOR in several malignancies, the question has been addressed whether mTOR operates through controlling of oncometabolite accumulation in metabolic reprogramming.
methodsHT-1080 cells - carrying originally endogenous IDH1 mutation - were used in vitro and in vivo. Anti-tumour effects of rapamycin were studied using different assays. The main sources and productions of the oncometabolites (2-HG and lactate) were analysed by
resultsRapamycin (mTORC1 inhibitor) inhibited proliferation, migration and altered the metabolic activity of IDH1 mutant HT-1080 cells. Rapamycin reduced the level of 2-HG sourced mainly from glutamine and glucose derived lactate which correlated to the decreased incorporation of
conclusionsConsidering the role of lactate and 2-HG in regulatory network and in metabolic symbiosis it could be assumed that mTOR inhibitors have additional effects besides their anti-proliferative effects in tumours with glycolytic phenotype, especially in case of IDH1 mutation (e.g. acute myeloid leukemias, gliomas, chondrosarcomas). Based on our new results, we suggest targeting mTOR activity depending on the metabolic and besides molecular genetic phenotype of tumours to increase the success of therapies.
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