ArticleFrontiers in immunology2026
ESCO1 stabilizes NUFIP2 through acetylation-ubiquitination crosstalk to promote pancreatic cancer progression.
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 is a highly aggressive malignancy with a poor prognosis, and its molecular pathogenesis remains incompletely understood, with effective therapeutic options still limited. Establishment of sister chromatid cohesion N-acetyltransferase 1 (ESCO1) has been implicated in the development and progression of several malignancies; however, its biological role and underlying mechanisms in pancreatic cancer remain largely unknown. This study aimed to elucidate the clinical significance and molecular mechanisms of the ESCO1/NUFIP2 axis in pancreatic cancer. Methods: TCGA, CPTAC, and other publicly available datasets were used to evaluate the expression patterns, diagnostic value, and prognostic significance of ESCO1 and NUFIP2 in pancreatic cancer. Results: ESCO1 and NUFIP2 were significantly upregulated in pancreatic cancer and were associated with poor prognosis. Functional assays demonstrated that the ESCO1/NUFIP2 axis promoted pancreatic cancer cell proliferation and migration, enhanced tumor growth Conclusion: ESCO1 stabilizes NUFIP2 through acetylation-dependent regulation, thereby preserving mitochondrial function, suppressing mitochondrial apoptosis, and promoting pancreatic cancer progression. The ESCO1/NUFIP2 axis may also contribute to the regulation of antitumor immunity, highlighting its potential as a biomarker and therapeutic target in pancreatic cancer.
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