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Related Experiment Video

Updated: Feb 2, 2026

Application of MassSQUIRM for Quantitative Measurements of Lysine Demethylase Activity

Application of MassSQUIRM for Quantitative Measurements of Lysine Demethylase Activity

Published on: March 11, 2012

Histone Demethylase KDM4B Promotes DNA Damage by Activating Long Interspersed Nuclear Element-1.

Ying Xiang¹, Kai Yan², Qian Zheng^1,3

¹School of Basic Medical Sciences, Wuhan University, Wuhan, China.

Cancer Research

|November 22, 2018

Summary

This summary is machine-generated.

The histone demethylase KDM4B promotes cancer by increasing LINE-1 activity, leading to DNA damage and instability. Inhibiting KDM4B reduces LINE-1 expression and damage, offering new therapeutic strategies.

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Area of Science:

Epigenetics
Cancer Biology
Genomics

Background:

Histone demethylase KDM4B is overexpressed in many cancers.
KDM4B's oncogenic role is linked to H3K9me3 demethylation, affecting gene expression and genome stability.
Global analysis of KDM4B's effect on H3K9me3 distribution was lacking.

Purpose of the Study:

To investigate the genome-wide effect of KDM4B on H3K9me3 distribution.
To determine KDM4B's role in regulating LINE-1 elements.
To explore the therapeutic potential of KDM4B inhibition in cancer.

Main Methods:

Genome-wide analysis of H3K9me3 distribution in cancer cells.
Assessment of LINE-1 expression and retrotransposition activity under varying KDM4B levels.
Pharmacologic inhibition of KDM4B in breast cancer cell lines.

Main Results:

H3K9me3 is enriched in long interspersed nuclear element-1 (LINE-1) regions.
KDM4B directly regulates LINE-1 expression and retrotransposition, particularly in young LINE-1 elements.
KDM4B overexpression enhances LINE-1 copy number, retrotransposition, and associated DNA damage.
High KDM4B levels in breast cancer correlate with increased LINE-1 activity and DNA damage.
KDM4B inhibition reduces LINE-1 expression and DNA damage in relevant cancer cells.

Conclusions:

KDM4B is a novel regulator of LINE-1 retrotransposition.
KDM4B overexpression contributes to tumorigenesis through LINE-1-induced DNA damage.
Targeting KDM4B offers a potential strategy for cancer prevention and therapy.