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Updated: May 7, 2026

RNA-Associated Chromatin DNA-DNA Interaction Method
Published on: April 30, 2026
A novel non-coding RNA lncRNA-JADE connects DNA damage signalling to histone H4 acetylation
Guohui Wan1, Xiaoxiao Hu, Yunhua Liu
1Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Abstract:
A prompt and efficient DNA damage response (DDR) eliminates the detrimental effects of DNA lesions in eukaryotic cells. Basic and preclinical studies suggest that the DDR is one of the primary anti-cancer barriers during tumorigenesis. The DDR involves a complex network of processes that detect and repair DNA damage, in which long non-coding RNAs (lncRNAs), a new class of regulatory RNAs, may play an important role. In the current study, we identified a novel lncRNA, lncRNA-JADE, that is induced after DNA damage in an ataxia-telangiectasia mutated (ATM)-dependent manner. LncRNA-JADE transcriptionally activates Jade1, a key component in the HBO1 (human acetylase binding to ORC1) histone acetylation complex. Consequently, lncRNA-JADE induces histone H4 acetylation in the DDR. Markedly higher levels of lncRNA-JADE were observed in human breast tumours in comparison with normal breast tissues. Knockdown of lncRNA-JADE significantly inhibited breast tumour growth in vivo. On the basis of these results, we propose that lncRNA-JADE is a key functional link that connects the DDR to histone H4 acetylation, and that dysregulation of lncRNA-JADE may contribute to breast tumorigenesis.
Insights
A novel long non-coding RNA, lncRNA-JADE, is activated by DNA damage and promotes breast tumor growth by enhancing histone acetylation. Its dysregulation may drive tumorigenesis, offering a potential therapeutic target.
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- DNA damage response (DDR) is crucial for preventing cancer.
- Long non-coding RNAs (lncRNAs) are emerging regulators in cellular processes.
- The role of lncRNAs in DDR and tumorigenesis is under investigation.
Purpose of the Study:
- To identify novel lncRNAs involved in the DNA damage response.
- To elucidate the function of lncRNA-JADE in DNA damage and breast cancer.
- To investigate the mechanism by which lncRNA-JADE influences gene expression.
Main Methods:
- Identification of lncRNA-JADE via DNA damage induction.
- Analysis of lncRNA-JADE's dependence on ATM signaling.
- Assessment of lncRNA-JADE's effect on Jade1 and histone H4 acetylation.
- Evaluation of lncRNA-JADE expression in human breast tumors.
- In vivo studies using lncRNA-JADE knockdown in mouse models.
Main Results:
- A novel lncRNA, lncRNA-JADE, was identified and found to be induced by DNA damage in an ATM-dependent manner.
- lncRNA-JADE transcriptionally activates Jade1, leading to increased histone H4 acetylation.
- Elevated lncRNA-JADE levels were detected in human breast tumors compared to normal tissues.
- Knockdown of lncRNA-JADE significantly suppressed breast tumor growth in vivo.
Conclusions:
- lncRNA-JADE acts as a critical link between the DNA damage response and histone acetylation.
- Dysregulation of lncRNA-JADE contributes to breast tumorigenesis.
- lncRNA-JADE represents a potential diagnostic marker and therapeutic target for breast cancer.
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