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May 27, 2026Cell Death DiscoveryOpen Access

ATP2B4 driven chromatin compaction exacerbates pancreatic cancer radiotherapy resistance

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Authors

YLY F LuoWJWei JiangYLYanfang Liu

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Overview

Randomized trial identifies ATP2B4's role in enhancing radiotherapy resistance in pancreatic cancer, suggesting it as a therapeutic target.

Key Points

  • This research aims to elucidate the molecular mechanisms contributing to radiotherapy resistance in pancreatic cancer cells, focusing on ATP2B4.
  • Utilized high-throughput metabolic CRISPR library screening and RNA sequencing to identify ATP2B4's role.
  • Performed micrococcal nuclease assays, drug rescue assays, and overexpression/silencing experiments to assess chromatin dynamics.
  • Conducted TurboID-based mass spectrometry and immunoprecipitation to investigate ATP2B4's mechanism of action.
  • Knockout of ATP2B4 caused chromatin decompaction and increased RT-induced cell apoptosis (p<0.001).
  • ATP2B4 was found to stabilize ELAVL1, affecting mRNA stability of histone H1.0, thereby impacting DNA damage response.
  • Identified ATP2B4 as a potential biomarker for radiotherapy outcomes, with significant implications for therapeutic targeting.

Cite This Study

Luo et al. (2026) studied this question.

synapsesocial.com/papers/6a1689eb0c924ddd1bd58a43https://doi.org/10.1038/s41420-026-03142-7
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