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Updated: Sep 10, 2025

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

33.8K

KDM4 Orchestrates Epigenomic Remodeling of Senescent Cells and Potentiates the Senescence-Associated Secretory

Boyi Zhang1, Qilai Long2, Shanshan Wu1

  • 1Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.

Aging Cell
|August 24, 2025
PubMed

Insights

Cellular senescence, a cancer-restraining process, involves KDM4 expression and altered methylation. Targeting KDM4 dampens the senescence-associated secretory phenotype (SASP), aiding cancer therapy and improving survival.

Area of Science:

  • Cellular and Molecular Biology
  • Oncology
  • Epigenetics

Background:

  • Cellular senescence is a critical mechanism that prevents neoplastic cell proliferation.
  • The role of specific epigenetic regulators, like KDM4, in senescence and cancer remains incompletely understood.

Purpose of the Study:

  • To investigate the role of KDM4 in cellular senescence and its impact on the tumor microenvironment.
  • To explore KDM4 targeting as a therapeutic strategy in prostate cancer.

Main Methods:

  • Assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) for global chromatin accessibility.
  • RNA sequencing for transcriptomic profiling.
  • In vivo and in vitro models of senescence and cancer.

Main Results:

  • KDM4 expression is upregulated during human stromal cell senescence.
  • Decreased H3K9/H3K36 methylation and altered chromatin accessibility correlate with poor patient survival in prostate cancer.
  • KDM4 inhibition reduces SASP, enhances cancer cell apoptosis, and improves survival in experimental models.

Conclusions:

  • Dynamic epigenetic changes, including H3K9/H3K36 methylation shifts, characterize senescence.
  • KDM4 is a key regulator of the senescence-associated secretory phenotype (SASP).
  • Targeting KDM4 offers a novel therapeutic approach to modulate senescence in cancer treatment.
Keywords:
H3K9/H3K36 demethylationKDM4age‐related pathologyagingcellular senescenceepigenetic modification

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