ArticleBreast cancer research and treatment2019
S-adenosylmethionine biosynthesis is a targetable metabolic vulnerability of cancer stem cells.
Article in Breast cancer research and treatment, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 80 citations in OpenAlex.
- Regional HNSCC metabolomics reveals widespread changes to one-carbon metabolism and S-adenosylmethionine metabolism across tumour core, tumour edge and adjacent non-tumour tissues.British journal of cancer · 2026Article
- Role of methionine metabolism in cancer: recent advances in molecular mechanisms and therapeutic implications.Experimental hematology & oncology · 2026Review
- One-carbon metabolism in cancer immunity: T-cell fitness, epigenetic programming, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Discovery of Potential Scaffolds for Methionine Adenosyltransferase 2A (MAT2A) Inhibitors: Virtual Screening, Synthesis, and Biological Evaluation.Molecules (Basel, Switzerland) · 2025Article
- Methionine Dependency and Restriction in Cancer: Exploring the Pathogenic Function and Therapeutic Potential.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Bridging epigenomics and tumor immunometabolism: molecular mechanisms and therapeutic implications.Molecular cancer · 2025Review
- Mechanisms and rationales of SAM homeostasis.Trends in biochemical sciences · 2025Review
- Tumor-initiating and metastasis-initiating cells of clear-cell renal cell carcinoma.Journal of biomedical science · 2025Review
- Article
- 8-Cl-Ado and 8-NHLeukemia · 2024Article
- Dietary methionine restriction in cancer development and antitumor immunity.Trends in endocrinology and metabolism: TEM · 2024Review
- Targeting EMSY-mediated methionine metabolism is a potential therapeutic strategy for triple-negative breast cancer.Cell reports. Medicine · 2024Article
- Characterization of methionine dependence in melanoma cells.Molecular omics · 2024Article
- Interplay between epigenetics and metabolism controls cancer stem cell plasticity.Frontiers in epigenetics and epigenomics · 2024Review
- Emerging roles of small extracellular vesicles in metabolic reprogramming and drug resistance in cancers.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- The Role of Amino Acids in the Diagnosis, Risk Assessment, and Treatment of Breast Cancer: A Review.Current issues in molecular biology · 2023Review
- Methionine orchestrates the metabolism vulnerability in cisplatin resistant bladder cancer microenvironment.Cell death & disease · 2023Article
- The Transcriptional and Epigenetic Landscape of Cancer Cell Lineage Plasticity.Cancer discovery · 2023Review
- Gluconeogenic enzyme PCK1 supports S-adenosylmethionine biosynthesis and promotes H3K9me3 modification to suppress hepatocellular carcinoma progression.The Journal of clinical investigation · 2023Article
- Cancer stem cell fate determination: mito-nuclear communication.Cell communication and signaling : CCS · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
purposeMany transformed cells and embryonic stem cells are dependent on the biosynthesis of the universal methyl-donor S-adenosylmethionine (SAM) from methionine by the enzyme MAT2A to maintain their epigenome. We hypothesized that cancer stem cells (CSCs) rely on SAM biosynthesis and that the combination of methionine depletion and MAT2A inhibition would eradicate CSCs.
methodsHuman triple (ER/PR/HER2)-negative breast carcinoma (TNBC) cell lines were cultured as CSC-enriched mammospheres in control or methionine-free media. MAT2A was inhibited with siRNAs or cycloleucine. The effects of methionine restriction and/or MAT2A inhibition on the formation of mammospheres, the expression of CSC markers (CD44
resultsMethionine restriction inhibited mammosphere formation and reduced the CD44
conclusionsOur findings point to SAM biosynthesis as a unique metabolic vulnerability of CSCs that can be targeted by combining methionine depletion with MAT2A inhibition to eradicate drug-resistant CSCs.
Indexed as
Identifiers
What OpenQuestion holds
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.