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SLMO2 inhibits apoptosis in ovarian cancer cells by modulating mitochondrial function via TRIAP1

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dc.contributor.authorYuesong Wang
dc.contributor.authorZixuan Li
dc.contributor.authorTianmei Zhang
dc.contributor.authorYaqi Wang
dc.contributor.departmentBiología Celular e Histología
dc.date.accessioned2026-02-16T15:51:58Z
dc.date.available2026-02-16T15:51:58Z
dc.date.issued2026
dc.description.abstractObjective. This study aimed to investigate the role of SLMO2 in regulating mitochondrial function and its interaction with TRIAP1, which inhibited apoptosis in ovarian cancer cells. The findings provided valuable insights into potential therapeutic targets for ovarian cancer. Methods. Lentiviral infection models were developed using SKOV3 and OVCAR3 ovarian cancer cell lines. Techniques such as flow cytometry, western blotting, immunofluorescence, and transmission electron microscopy were employed to systematically assess the regulatory effects of SLMO2 and TRIAP1 on cell proliferation, apoptosis, mitochondrial function, and autophagy. Additionally, a subcutaneous mouse tumor xenograft model was utilized to further investigate the combined effects of SLMO2 and TRIAP1 on ovarian cancer cells, with the aim of elucidating the specific mechanisms underlying tumor growth and apoptosis. Results. SLMO2 enhanced mitochondrial function by increasing membrane potential and reducing reactive oxygen species (ROS) levels. Furthermore, through its interaction with TRIAP1, SLMO2 inhibited autophagy, which further suppressed apoptosis in ovarian cancer cells and regulated mitochondrial function. In vivo experiments showed decreased ROS levels and reduced expression of autophagy-related proteins, further supporting the roles of SLMO2 and TRIAP1 in the regulation of mitochondrial function. Conclusions. SLMO2 regulated mitochondrial function and inhibited apoptosis in ovarian cancer cells by interacting with TRIAP1. The combination of SLMO2 and TRIAP1 promoted tumor cell growth and induced oxidative stress, suggesting potential therapeutic targets for ovarian cancer.
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dc.format.extent14
dc.identifier.doihttps://doi.org/10.14670/HH-18-958
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/206021
dc.languageeng
dc.relationUniversidad de Murcia, Departamento de Biologia Celular e Histiologia
dc.relationSin financiación externa a la Universidad
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectOvarian cancer
dc.subjectMitochondrial function
dc.subjectApoptosis inhibition
dc.subjectSLMO2-TRIAP1
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleSLMO2 inhibits apoptosis in ovarian cancer cells by modulating mitochondrial function via TRIAP1
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublication
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Histology and histopathology, Vol.41, Nº3, (2026)