ArticleCancer research2024
E-Cadherin Induces Serine Synthesis to Support Progression and Metastasis of Breast Cancer.
Article in Cancer research, 2024. 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.
- PHGDH in cancer: a narrative review of its functions beyond serine metabolism.Translational cancer research · 2026Review
- A 3D-Printed Vascular-Like Perfusion Tumor-on-a-Chip Recapitulates High-Grade Breast Cancer With in Vivo-Relevant Drug Resistance.Advanced healthcare materials · 2026Article
- The MAPK/ATF3/ASNS axis drives amino acid metabolic reprogramming to promote NSCLC survival under glucose deprivation.Journal of translational medicine · 2026Article
- Necroptosis triggers inflammatory interferon signatures in patient-derived metastatic breast cancer organoids.Signal transduction and targeted therapy · 2026Article
- Metabolic maintenance of breast cancer cells and metastases through E-cadherin/YAP-dependent pyruvate carboxylase expression.bioRxiv : the preprint server for biology · 2026Article
- Soluble E-cadherin-CXCL1-CXCR2 axis as a therapeutic vulnerability in inflammatory breast cancer brain metastasis.Neuro-oncology · 2026Article
- Lactobacillus crispatus attenuates Escherichia coli-induced inflammation and migration of cervical cancer cells.AMB Express · 2026Article
- E-cadherin expression promotes tumor growth via KLRG1-dependent pathways.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- TTPAL inhibits the progression of breast cancer and reprograms tumor-associated macrophages by inhibiting JAK2/STAT3 signaling pathway.Breast cancer research : BCR · 2026Article
- T‑cadherin and its impact on human diseases (Review).Molecular medicine reports · 2026Review
- 3D "Emboli" Culture Models Epithelial Breast Cancer Cell Oxidative Mitochondrial Metabolism with Relevance for Lung Metastasis.Cancer research communications · 2026Article
- Hypoxia-Driven Pulmonary Adaptation in the Yak: A Homeostatic Mechanism Mediated by Cell Adhesion Molecules.International journal of molecular sciences · 2026Article
- Dendrobine inhibits anaplastic thyroid cancer progression by targeting the JAK-STAT3 pathway.Frontiers in oncology · 2026Article
- One-carbon metabolism in cancer immunity: T-cell fitness, epigenetic programming, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Machine learning-based signature for prognosis and drug sensitivity in hepatocellular carcinoma using glycolysis-related gene.Oncology letters · 2026Article
- The "serine code" of metabolic reprogramming: multidimensional roles of the serine synthesis pathway in tumors and novel breakthroughs for targeted therapy.Frontiers in immunology · 2026Review
- Gastric metastasis from hormone receptor-positive breast cancer ten years after radical mastectomy: a case report and literature review.Frontiers in oncology · 2026Article
- Photothermal Combination Therapy for Metastatic Breast Cancer: A New Strategy and Future Perspectives.Biomedicines · 2025Review
- Interplay between malic enzyme 2, de novo serine synthesis, and the malate-aspartate shuttle drives metabolic adaptation in triple-negative breast cancer.Cancer & metabolism · 2025Article
- Mesenchymal-epithelial transition reduces proliferation but increases immune evasion in tumor spheroids.iScience · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
The loss of E-cadherin, an epithelial cell adhesion molecule, has been implicated in metastasis by mediating the epithelial-mesenchymal transition, which promotes invasion and migration of cancer cells. However, recent studies have demonstrated that E-cadherin supports the survival and proliferation of metastatic cancer cells. Here, we identified a metabolic role for E-cadherin in breast cancer by upregulating the de novo serine synthesis pathway (SSP). The upregulated SSP provided metabolic precursors for biosynthesis and resistance to oxidative stress, enabling E-cadherin+ breast cancer cells to achieve faster tumor growth and enhanced metastases. Inhibition of phosphoglycerate dehydrogenase, a rate-limiting enzyme in the SSP, significantly and specifically hampered proliferation of E-cadherin+ breast cancer cells and rendered them vulnerable to oxidative stress, inhibiting their metastatic potential. These findings reveal that E-cadherin reprograms cellular metabolism, promoting tumor growth and metastasis of breast cancers. Significance: E-Cadherin promotes the progression and metastasis of breast cancer by upregulating the de novo serine synthesis pathway, offering promising targets for inhibiting tumor growth and metastasis in E-cadherin-expressing tumors.
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