ArticleTranslational oncology2025
SIRT5 inhibits glycolysis and nasal type extranodal NK/T cell lymphoma cell proliferation by catalyzing the desuccinylation of glucose-6-phosphate isomerase.
Article in Translational oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Mechanistic and functional integration of sirtuin deacylases: from substrate specificity to biological outcomes.Glycoconjugate journal · 2026Review
- Beyond deacetylation: crosstalk mechanisms and context-dependent regulation of sirtuin non-classical enzymatic functions in disease.Molecular medicine (Cambridge, Mass.) · 2026Review
- Balsalazide-Derived Heterotriaryls as Sirtuin 5 Inhibitors: A Case Study of a Reversible Covalent Inhibition Strategy.Molecules (Basel, Switzerland) · 2025Article
- Regulators of Cancer Progression: Succinylation.Cancers · 2025Review
- Sirtuins and tumor immunity: mechanistic insights, immunotherapy prospects, and therapeutic horizons.Frontiers in immunology · 2025Review
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Authors and funding
6 authors.
Funding
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Abstract
backgroundExtranodal natural killer/T-cell lymphoma, nasal type (ENKTL) is a malignant tumor harboring a poor prognosis and unsatisfactory treatment outcomes. This study was performed to explore the pathogenesis and exact etiology of ENKTL. Methods Bioinformatic analysis was conducted to investigate the expression of SIRT5 and glucose-6-phosphate isomerase (GPI), as well their correlation with ENKTL overall survival. Cell proliferation ability and cell apoptosis were determined by CCK8, soft-agar colony formation and Tunel assays. Pyruvic acid and lactate production, GPI activity and F6P levels were detected to indicate glycolysis process. Succinylation modification in GPI protein was quantified by 4D label-free succinylation modification quantitative proteome. ENKTL mouse model was established by the injection of SNK6 cells.
resultsSIRT5 suppressed the NKTL cell proliferation through the desuccinylation effect, while it was down-regulated in the ENKTL. SIRT5 catalyzed the desuccinylation of glycolytic enzyme GPI in ENKTL cells, which accelerated GPI protein degradation through the autophagy-lysosome system. SIRT5 inhibited glycolysis via mediating the desuccinylation of GPI, thereby suppressing ENKTL cell proliferation. The antitumor role of SIRT5 was also certified in ENKTL mouse model by targeting GPI.
conclusionSIRT5 inhibits glycolysis via catalyzed the desuccinylation of glycolytic enzyme GPI, thereby repressing ENKTL cells proliferation and tumor growth. As SIRT5 serves as a tumor suppressor in ENKTL, it may be a promising molecular target in therapy strategy.
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