ArticleCell & bioscience2023
SHMT2 regulates esophageal cancer cell progression and immune Escape by mediating m6A modification of c-myc.
Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Epitranscriptomic Regulation of ALDOA by SHMT2-Mediated m6A Modification Drives Gastric Cancer Malignancy.Molecular carcinogenesis · 2026Article
- Serine Hydroxymethyltransferase (SHMT) in biology and disease: molecular mechanisms and therapeutic targeting.Journal of translational medicine · 2026Review
- ADAMDEC1-driven CCL2-CCR2-PD-1 axis in esophageal squamous cell carcinoma: a dual threat of O-GlcNAcylation and mCellular oncology (Dordrecht, Netherlands) · 2026Article
- Advances in epigenetic therapy for esophageal cancer.Clinical epigenetics · 2026Review
- Development and validation of an m6A and autophagy related lncRNAs signature for predicting survival and modulating the immune microenvironment in esophageal squamous cell carcinoma.Frontiers in immunology · 2026Article
- Advances in research on RNA methylation and its role in the immune microenvironment of gastrointestinal tumors.Frontiers in cell and developmental biology · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- Article
- RNA Methylation in Cancer Metabolism: from Mechanisms to Therapeutic Opportunities.International journal of biological sciences · 2026Review
- Article
- Unveiling the role of m6A modification in esophageal cancer: a new frontier in tumor innate interferon immunity.Cancer cell international · 2025Review
- The mMolecular biomedicine · 2025Review
- Article
- Molecular classification and construction of the risk signature for diffuse large B-cell lymphoma based on vitamin B6 metabolism.Discover oncology · 2025Article
- Biological roles of enhancer RNA m6A modification and its implications in cancer.Cell communication and signaling : CCS · 2025Review
- Serine Hydroxymethyltransferase Modulates Midgut Physiology inBiomolecules · 2025Article
- Role of the mInternational journal of molecular medicine · 2025Review
- Exploring metabolic reprogramming in esophageal cancer: the role of key enzymes in glucose, amino acid, and nucleotide pathways and targeted therapies.Cancer gene therapy · 2025Review
- RNA Modification and Digestive Tract Tumors: A Review.Current medicinal chemistry · 2025Review
- Role and mechanisms of m6A demethylases in digestive system tumors.American journal of cancer research · 2025Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn recent years, the role of altered cellular metabolism in tumor progression has attracted widespread attention. Related metabolic enzymes have also been considered as potential cancer therapeutic targets. Serine hydroxymethyltransferase 2 (SHMT2) has been reported to be upregulated in several cancers and associated with poor prognosis. However, there are few studies of SHMT2 in esophageal cancer (EC), and the related functions and mechanisms also need to be further explored.
methodsIn this study, we first analyzed SHMT2 expression in EC by online database and clinical samples. Then, the biological functions of SHMT2 in EC were investigated by cell and animal experiments. The intracellular m6A methylation modification levels were also evaluated by MeRIP. Linked genes and mechanisms of SHMT2 were analyzed by bioinformatics and rescue experiments.
resultsWe found that SHMT2 expression was abnormally upregulated in EC and associated with poor prognosis. Functionally, SHMT2 silencing suppressed c-myc expression in an m6A-dependent manner, thereby blocking the proliferation, migration, invasion and immune escape abilities of EC cells. Mechanistically, SHMT2 encouraged the accumulation of methyl donor SAM through a one-carbon metabolic network, thereby regulating the m6A modification and stability of c-myc mRNA in a METTL3/FTO/ALKBH5/IGF2BP2-dependent way. In vivo animal experiments also demonstrated that SHMT2 mediated MYC expression by m6A-methylation modification, thus boosting EC tumorigenesis.
conclusionIn conclusion, our data illustrated that SHMT2 regulated malignant progression and immune escape of EC cell through c-myc m6A modification. These revealed mechanisms related to SHMT2 in EC and maybe offer promise for the development of new therapeutic approaches.
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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.