ArticleNature communications2024
Wild-type IDH2 is a therapeutic target for triple-negative breast cancer.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 24 citations in OpenAlex.
- Comutation of asxl1 and IDH2R172K enhances leukemogenesis and correlates with epigenetic activation of MAPK and AP-1 in zebrafish.Blood advances · 2026Article
- Article
- Emerging roles of RNA mInternational journal of oncology · 2026Review
- Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer.Current oncology (Toronto, Ont.) · 2026Review
- CBFA2T2: a novel H3K27 reader regulating metabolism and tumor growth.Molecular cancer · 2026Article
- Reversible arginine methylation regulates mitochondrial IDH2 activity: coordinated control by CARM1 and KDM3A/4A.Cell death & disease · 2026Article
- Dual Targeting of IDH2 and the Ubiquitin-Proteasome System Reveals a Functional Vulnerability in Breast Cancer Models.Cancers · 2026Article
- Hepatic mitochondrial signaling as a systemic hub: inter-organ communication networks in aging and aging-related diseases.Frontiers in cell and developmental biology · 2026Review
- The multifaceted roles of mitochondria and their therapeutic transformation: a new perspective on triple-negative breast cancer treatment.Frontiers in oncology · 2026Article
- SIRT3-IDH2 axis is a target of dietary fructose: implication of IDH2 as a key player in dietary carcinogen toxicity in mice colon.Experimental & molecular medicine · 2025Article
- Celastrol inhibits the DPYSL2-JAK/STAT pathway by targeting mito-IDHs mediated mitochondrial metabolism to exhaust breast cancer.Acta pharmacologica Sinica · 2025Article
- Prefoldin complex promotes interferon-stimulated gene expression and is inhibited by rotavirus VP3.Nature communications · 2025Article
- Article
- The Role of N6-Methyladenosine in Mitochondrial Dysfunction and Pathology.International journal of molecular sciences · 2025Review
- Metabolic Profiling of Breast Cancer Cell Lines: Unique and Shared Metabolites.International journal of molecular sciences · 2025Article
- A review of the pathogenesis of mitochondria in breast cancer and progress of targeting mitochondria for breast cancer treatment.Journal of translational medicine · 2025Review
- The Ku70-SIX1-GPT2 axis regulates alpha-ketoglutarate metabolism to drive progression of prostate cancer.Oncogene · 2025Article
- Investigating the relationship between blood metabolites and diabetic retinopathy using two-sample mendelian randomization and in vivo validation.Scientific reports · 2024Article
- Article
- Allergen-specific sublingual immunotherapy altered gut microbiota in patients with allergic rhinitis.Frontiers in cellular and infection microbiology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in isocitrate dehydrogenases (IDH) are oncogenic events due to the generation of oncogenic metabolite 2-hydroxyglutarate. However, the role of wild-type IDH in cancer development remains elusive. Here we show that wild-type IDH2 is highly expressed in triple negative breast cancer (TNBC) cells and promotes their proliferation in vitro and tumor growth in vivo. Genetic silencing or pharmacological inhibition of wt-IDH2 causes a significant increase in α-ketoglutarate (α-KG), indicating a suppression of reductive tricarboxylic acid (TCA) cycle. The aberrant accumulation of α-KG due to IDH2 abrogation inhibits mitochondrial ATP synthesis and promotes HIF-1α degradation, leading to suppression of glycolysis. Such metabolic double-hit results in ATP depletion and suppression of tumor growth, and renders TNBC cells more sensitive to doxorubicin treatment. Our study reveals a metabolic property of TNBC cells with active utilization of glutamine via reductive TCA metabolism, and suggests that wild-type IDH2 plays an important role in this metabolic process and could be a potential therapeutic target for TNBC.
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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.