ArticleCancer & metabolism2019
Epithelial to mesenchymal transition (EMT) is associated with attenuation of succinate dehydrogenase (SDH) in breast cancer through reduced expression of
Article in Cancer & metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
- Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer.Current oncology (Toronto, Ont.) · 2026Review
- Altered Expression of Mitochondrial Succinate Dehydrogenase Subunit D Influences Breast Cancer Progression.International journal of molecular sciences · 2026Article
- Assessment of the anticancer and antimetastatic effects of monocarbonyl analogs of curcumin, C66 and B2BrBC, in breast cancer cells.Cancer cell international · 2026Article
- Mapping of Functional Metabolic Phenotypes in Acute Myeloid Leukemia.Cancer medicine · 2025Article
- Selenoprotein O Promotes Melanoma Metastasis and Regulates Mitochondrial Complex II Activity.Cancer research · 2025Article
- The prowess of metabolomics in cancer research: current trends, challenges and future perspectives.Molecular and cellular biochemistry · 2025Review
- Twist-Induced Epithelial-to-Mesenchymal Transition Confers Specific Metabolic and Mitochondrial Alterations.Cells · 2025Article
- Exploring the critical role of SDHA in breast cancer proliferation: implications for novel therapeutic strategies.American journal of translational research · 2025Article
- The role of cytidine 5'-triphosphate synthetase 1 in metabolic rewiring during epithelial-to-mesenchymal transition in non-small-cell lung cancer.FEBS open bio · 2024Article
- Th17 cells target the metabolic miR-142-5p-succinate dehydrogenase subunit C/D (SDHC/SDHD) axis, promoting invasiveness and progression of cervical cancers.Molecular oncology · 2024Article
- Tricarboxylic Acid Cycle Relationships with Non-Metabolic Processes: A Short Story with DNA Repair and Its Consequences on Cancer Therapy Resistance.International journal of molecular sciences · 2024Review
- Targeting valine catabolism to inhibit metabolic reprogramming in prostate cancer.Cell death & disease · 2024Article
- Deficiency of SDHC promotes metastasis by reprogramming fatty acid metabolism in colorectal cancer.Journal of translational medicine · 2024Article
- Mitochondrial inhibitors: a new horizon in breast cancer therapy.Frontiers in pharmacology · 2024Review
- Stromal-Modulated Epithelial-to-Mesenchymal Transition in Cancer Cells.Biomolecules · 2023Review
- Targeting Mitochondrial Metabolic Reprogramming as a Potential Approach for Cancer Therapy.International journal of molecular sciences · 2023Review
- Succinate dehydrogenase complex subunit C: Role in cellular physiology and disease.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- circCAPRIN1 interacts with STAT2 to promote tumor progression and lipid synthesis via upregulating ACC1 expression in colorectal cancer.Cancer communications (London, England) · 2023Article
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Authors and funding
20 authors at 7 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpithelial to mesenchymal transition (EMT) is a well-characterized process of cell plasticity that may involve metabolic rewiring. In cancer, EMT is associated with malignant progression, tumor heterogeneity, and therapy resistance. In this study, we investigated the role of succinate dehydrogenase (SDH) as a potential key regulator of EMT.
methodsAssociations between SDH subunits and EMT were explored in gene expression data from breast cancer patient cohorts, followed by in-depth studies of SDH suppression as a potential mediator of EMT in cultured cells.
resultsWe found an overall inverse association between EMT and the SDH subunit C (SDHC) when analyzing gene expression in breast tumors. This was particularly evident in carcinomas of basal-like molecular subtype compared to non-basal-like tumors, and a low
conclusionsOur findings suggest that downregulation of SDHC promotes EMT and that this is accompanied by structural remodeling of the mitochondrial organelles. This may confer survival benefits upon exposure to hostile microenvironment including oxidative stress and hypoxia during cancer progression.
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