ArticleFrontiers in immunology2026
VEZT promotes pancreatic cancer progression by stabilizing SLC25A24 and preserving mitochondrial function.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pancreatic cancer (PC) is a highly aggressive malignancy with an unclear pathogenesis, limited therapeutic options, and poor prognosis. Vezatin (VEZT), an adherens junction transmembrane protein, has been implicated in the development and progression of several malignancies, including gastric cancer. However, its biological role and underlying mechanisms in pancreatic cancer remain largely unexplored. This study aimed to investigate the role of VEZT in pancreatic cancer progression and elucidate the molecular mechanism by which VEZT regulates mitochondrial homeostasis through Solute Carrier Family 25 Member 24 (SLC25A24), thereby suppressing apoptosis and promoting malignant progression. Methods: The expression patterns and clinical significance of VEZT and SLC25A24 were analyzed using public datasets from TCGA and GTEx. Their biological functions were systematically evaluated through a series of Results: VEZT and SLC25A24 were both significantly upregulated in pancreatic cancer tissues, and their elevated expression was closely associated with unfavorable patient prognosis. Both molecules also exhibited good diagnostic performance. Immune infiltration analysis showed that the expression levels of VEZT and SLC25A24 were significantly associated with multiple tumor-infiltrating immune cell populations. Functional assays demonstrated that VEZT knockdown markedly inhibited pancreatic cancer cell proliferation, colony formation, migration, and invasion, while promoting apoptosis; restoration of SLC25A24 expression partially reversed these effects. Further investigations revealed a protein interaction between VEZT and SLC25A24. VEZT knockdown reduced the stability and expression level of SLC25A24 protein and was accompanied by impaired mitochondrial function. Conclusions: This study reveals the oncogenic role of VEZT in pancreatic cancer and identifies SLC25A24 as an important downstream effector. The VEZT/SLC25A24 axis may promote pancreatic cancer progression by modulating mitochondrial function and apoptosis, highlighting its potential value for prognostic assessment and therapeutic targeting.
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