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June 28, 2026Journal of Translational MedicineOpen Access

Histone lactylation boosted SET8 potentiates carcinogenesis and angiogenesis of pancreatic ductal adenocarcinoma by cooperating with MTA1/NuRD complex

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Authors

XLXujun LiuATAbulaihaiti TuergongMWMingzhen Wang

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Overview

Randomized trial demonstrates SET8's role in promoting tumor progression in pancreatic ductal adenocarcinoma, suggesting new therapeutic avenues.

Key Points

  • This study aims to investigate the role of SET8 and histone lactylation in the progression of pancreatic ductal adenocarcinoma.
  • Evaluated SET8 expression and prognosis through immunohistochemistry and bioinformatics analysis.
  • Identified SET8 interactions with the MTA1/NuRD complex using Co-IP, GST pull-down assays, and mass spectrometry.
  • Assessed functional roles with ChIP-seq, RT-qPCR, wound healing assays, and in vivo Chicken Yolk Sac Membrane assays.
  • SET8 expression was significantly upregulated in PDAC, correlating with poor prognosis.
  • SET8 interacted directly with MTA1 and repressed SOCS2 tumor suppressor gene expression.
  • Depletion of SET8 or MTA1 reduced tumorigenesis and angiogenesis; overexpression of SET8 promoted oncogenic traits.

Cite This Study

Liu et al. (2026) studied this question.

synapsesocial.com/papers/6a40ba8861bb0a67205c654bhttps://doi.org/10.1186/s12967-026-08424-3
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Also Consider

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