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Updated: Jun 7, 2025

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

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Inhibition of bromodomain regulates cellular senescence in pancreatic adenocarcinoma

Xiang Chen1, Tao Yu1, Shu Li1

  • 1Department of Hepatobiliary Surgery, Affiliated Hospital of Jiujiang University Jiujiang 332000, Jiangxi, China.

International Journal of Clinical and Experimental Pathology
|November 15, 2024
PubMed
Abstract

Insights

The BET inhibitor JQ1 effectively reduced pancreatic cancer cell proliferation and induced senescence. JQ1 also inhibited epithelial-mesenchymal transition and Wnt signaling, offering potential new therapeutic targets for pancreatic cancer.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Bromodomain and extra terminal domain (BET) proteins are key epigenetic regulators.
  • The small molecule BET inhibitor JQ1 has shown efficacy in various cancers.
  • BET proteins influence gene transcription via acetylated histone interactions.

Purpose of the Study:

  • To investigate the therapeutic potential of JQ1 in pancreatic cancer.
  • To evaluate BRD4 protein expression in pancreatic cancer.
  • To analyze the correlation between BRD4 and clinicopathologic features and immune checkpoints.

Main Methods:

  • Investigated JQ1's effect on pancreatic adenocarcinoma (PAAD) cells.
  • Utilized GEPIA and Human Protein Atlas for BRD4 expression analysis.
  • Employed UALACN and TIMER databases to correlate BRD4 with clinical features and immune checkpoints.

Main Results:

  • JQ1 significantly inhibited PAAD cell proliferation and induced senescence.
  • JQ1 demonstrated minimal impact on the Senescence-associated secretory phenotype (SASP).
  • JQ1 effectively suppressed epithelial-mesenchymal transition (EMT) and Wnt signaling pathways.

Conclusions:

  • JQ1 exhibits anti-cancer properties in pancreatic cancer models.
  • JQ1's inhibition of EMT and Wnt pathways presents novel therapeutic avenues.
  • These findings support JQ1 as a potential therapeutic target for pancreatic cancer treatment.
Keywords:
EMTJQ1Pancreatic adenocarcinomaSASPsenescence

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