ArticleCell death & disease2021
ECHS1, an interacting protein of LASP1, induces sphingolipid-metabolism imbalance to promote colorectal cancer progression by regulating ceramide glycosylation.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- LIM and SH3 protein 1 deficiency confers resistance to cytotoxic lymphocyte-mediated lysis and immunotherapy in gastric cancer by disrupting cytoskeleton dynamics.Journal for immunotherapy of cancer · 2026Article
- Lipid-Soluble Signaling Molecular Model Predicts Prognosis and Immunotherapy Response in Gastric Cancer.Lipids · 2026Article
- TRAM-LAG1-CLN8 domain-containing protein TMEM56 regulates cell migration by changing intracellular ceramide levels.BMC biology · 2026Article
- Functional Analysis of Late-Onset Alzheimer's Disease Risk Genes inbioRxiv : the preprint server for biology · 2026Article
- Exploring Lipid Metabolic Reprogramming: Mechanistic Insights and Implications for Tumor Radiotherapy.International journal of biological sciences · 2026Review
- IFIT3 promotes lymph node metastasis by interacting with LASP1 to activate FAK-ERK signaling in esophageal squamous cell carcinoma.Cell death & disease · 2025Article
- Photodynamic therapy simultaneously induces ferroptosis- and apoptosis-like lipid signatures in ovarian cancer cells.Cell death & disease · 2025Article
- Immunoregulatory roles of post-translational modifications in colorectal cancer: mechanisms and therapeutic implications.Cellular and molecular life sciences : CMLS · 2025Review
- Prognostic and therapeutic implications related to glycosylation profiles of cancer-associated fibroblasts in colorectal cancer: insights from single-cell and bulk transcriptomics.Functional & integrative genomics · 2025Article
- ECHS1: pathogenic mechanisms, experimental models, and emerging therapeutic strategies.Orphanet journal of rare diseases · 2025Review
- Sugar symphony: glycosylation in cancer metabolism and stemness.Trends in cell biology · 2025Review
- Structural and biochemical mechanism of short-chain enoyl-CoA hydratase (ECHS1) substrate recognition.Communications biology · 2025Article
- Synthesis, function, and therapeutic potential of glycosphingolipids.Frontiers in immunology · 2025Review
- Neurological, metabolic and inflammatory phenotypes in a mouse model of ECHS1 deficiency.Brain communications · 2025Article
- ECHS1 as a Lipid Metabolism Biomarker for Pediatric Focal Segmental Glomerulosclerosis.PloS one · 2025Article
- Integrated bulk and single-cell profiling characterize sphingolipid metabolism in pancreatic cancer.BMC cancer · 2024Article
- Valine and Inflammation Drive Epilepsy in a Mouse Model of ECHS1 Deficiency.bioRxiv : the preprint server for biology · 2024Article
- METTL5 promotes gastric cancer progressionWorld journal of gastrointestinal oncology · 2024Article
- Therapeutic Potential for Sphingolipids in Inflammatory Bowel Disease and Colorectal Cancer.Cancers · 2024Review
- Expression and clinical significance of ECHS1 in gastric cancer.Journal of Cancer · 2024Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Sphingolipid metabolic dysregulation has increasingly been considered to be a drug-resistance mechanism for a variety of tumors. In this study, through an LC-MS assay, LIM and SH3 protein 1 (LASP1) was identified as a sphingolipid-metabolism-involved protein, and short-chain enoyl-CoA hydratase (ECHS1) was identified as a new LASP1-interacting protein through a protein assay in colorectal cancer (CRC). Gain- and loss-of-function analyses demonstrated the stimulatory role played by ECHS1 in CRC cell proliferation, migration, and invasion in vitro and in vivo. Mechanistic studies of the underlying tumor-supportive oncometabolism indicate that ECHS1 enables altering ceramide (Cer) metabolism that increases glycosphingolipid synthesis (HexCer) by promoting UDP-glucose ceramide glycosyltransferase (UGCG). Further analysis showed that ECHS1 promotes CRC progression and drug resistance by releasing reactive oxygen species (ROS) and interfering mitochondrial membrane potential via the PI3K/Akt/mTOR-dependent signaling pathway. Meanwhile, the phenomenon of promoting the survival and drug resistance of CRC cells caused by ECHS1 could be reversed by Eliglustat, a specific inhibitor of UCCG, in vitro and in vivo. IHC assay showed that ECHS1 was overexpressed in CRC tissues, which was related to the differentiation and poor prognosis of CRC patients. This study provides new insight into the mechanism by which phospholipids promote drug resistance in CRC and identifies potential targets for future therapies.
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