ArticleJournal of experimental & clinical cancer research : CR2025
SENP1 drives glycolysis and cisplatin resistance in gastric cancer via desumoylating ENO1.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- SENP7 mediates deSUMOylation and deubiquitination of SP1 to promote lung adenocarcinoma progression and chemoresistance.Translational oncology · 2026Article
- Review
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- Hesperidin and Hesperetin: Epigenetic-Stemness Crosstalk, Antitumor Mechanisms, Preclinical Data and Translation Barriers.Biomolecules · 2026Review
- Protein modification systems as cancer biomarkers and therapeutic targets.Precision clinical medicine · 2026Review
- ENO1 as a Central Regulator Linking Metabolic Reprogramming to Tumor Plasticity.International journal of molecular sciences · 2026Review
- SENP1 drives de novo cholesterogenesis via disrupting SUMOylation-mediated SREBP2-FBXW7 interaction.Cancer & metabolism · 2026Article
- ROS-SUMO Crosstalk in Oxidative Stress: Disease Mechanisms and Reproductive Health.Antioxidants (Basel, Switzerland) · 2026Review
- Glycolytic reprogramming in precancerous lesions of gastric cancer progression: pathogenesis and therapeutic potential.Frontiers in oncology · 2026Review
- An integrated network toxicology and multi-omics study identifies ENO1 as a candidate mediator in benzo[a]pyrene-related gastric cancer progression.Frontiers in pharmacology · 2026Article
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13 authors.
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Abstract
backgroundGastric cancer remains a leading cause of cancer-related mortality in world, with advanced-stage patients facing poor prognosis despite emerging therapies. SUMOylation modification is a major post-translation modification, which is essential for cellular behaviors. However, the potential function of SUMOylation in gastric cancer (GC) and the underlying molecular mechanisms remain unclear.
methodsIn our study, a bioinformatics analysis was conducted to screen potential regulators within the SUMO-Specific Peptidase (SENP) family in GC. In vitro functional experiments including CCK8, colony formation, transwell assay, sphere formation, Glycolytic flux, ECAR and OCR and several animal models including GC xenografts, organoids and lung metastasis models were employed to ascertain the role of SENP1 in GC progression and metastasis. Mass spectrometry analysis, coimmunoprecipitation and immunofluorescence staining were performed to elucidate the mechanisms by which SENP1 functions in GC cells.
resultsWe identified that SENP1 was upregulated in GC tissues and correlated with a poor prognosis. Multiple functional experiments demonstrated that SENP1 promotes the proliferation, migration, stemness and glycolysis of GC cells. Mechanistically, SENP1 binds to α-enolase (ENO1) and deSUMOylates the SUMO sites (K256, K394) of SUMO2-modified ENO1, enhancing ENO1 stability and drive gastric tumorigenesis. Meanwhile, SENP1 inhibitor Momordin Ιc (Mc) in combination with cisplatin has a synergistic effect on gastric tumor growth in vitro and in vivo.
conclusionSENP1 facilitates gastric cancer progression by metabolic reprogramming. Targeting SENP1 with Momordin Ic is a novel therapeutic approach for GC patients.
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