ArticleEuropean journal of medical research2025
SENP5 promotes endometrial cancer cell growth by regulating β-catenin deSUMOylation to enhance GPX4-resistance to ferroptosis.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- MGST3 Promotes Endometriosis Progression by Suppressing Ferroptosis.Cell biochemistry and biophysics · 2026Article
- Selenoproteins: Minute yet vital players governing cellular fate.Genes & diseases · 2026Review
- Remodeling the tumor microenvironment: regulatory effects of β-sitosterol and luteolin on the immunosuppressive milieu in endometrial carcinoma and implications for combinatorial immunotherapy.Frontiers in immunology · 2025Review
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7 authors.
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Abstract
backgroundEndometrial cancer (EC) is a significant and serious gynecological cancer, constituting a considerable risk to women's health. The desumoylation of SUMO specific peptidase 5 (SENP5) is intricately linked with various cancers. Nonetheless, the function of SENP5 in EC and its regulation of EC progression through the related mechanism of desumoylation modification remain elusive.
methodsFive samples of EC tumor tissues, along with para-cancerous tissues, were obtained. The expression of SENP5 in EC was assessed using reverse transcription-polymerase chain reaction (RT-qPCR), immunohistochemistry (IHC), and Western blot. HEC-1-B cells were treated with liposomes to interfere SENP5 and/or β-catenin expression. The methodologies employed to assess the impact of SENP5 on the proliferation of EC cells via β-catenin included RT-qPCR, Western blot, CCK8, EDU, and C11-BODIPY methods. Western blot, co-immunoprecipitation (CO-IP), and SUMOylation analysis were conducted to investigate the desumoylation modification of β-catenin by SENP5.
resultsSENP5 exhibited elevated expression levels in EC cancer tissues and was correlated with a negative prognosis for patients diagnosed with EC. The suppression of SENP5 inhibited the expression of β-catenin and GPX4, activated ferroptosis, and inhibited HEC-1-B -cell proliferation. Knockdown of β-catenin counteracted the impact of SENP5 overexpression on ferroptosis and HEC-1-B proliferation. In addition, SENP5 stabilized β-catenin level in HEC-1-B cells through desumoylation modification of the β-catenin protein.
conclusionsSENP5 promotes GPX4-mediated ferroptosis resistance, thereby enhancing the proliferation of EC cells by regulating β-catenin desumoylation, this finding indicates that SENP5 may serve as a promising target for therapeutic interventions in the treatment of EC.
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