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Author Spotlight: Epigenetic Modifications and Metabolic Rewiring as Targets for Cancer Therapy
Published on: October 18, 2024
Histone demethylase JMJD1A in cancer progression and therapeutic resistance
Hee-Young Jeon1,2, Hyunju Ryu1,2, Majid Pornour1,2
1Department of Biochemistry and Molecular Biology, University of Maryland, Baltimore, Maryland, USA.
Abstract:
JMJD1A (also called lysine demethylase 3A [KDM3A]) belongs to the Jumonji C family of histone demethylases. It specifically removes the repressive mono- or di-methyl marks from histone H3 at lysine 9 and thus contributes to the activation of gene transcription. JMJD1A plays a key role in a variety of biological processes such as spermatogenesis, metabolism, sex determination, and stem cell activity. JMJD1A is upregulated in various types of cancers and can promote cancer development, progression, and therapeutic resistance. JMJD1A can epigenetically regulate the expression or activity of transcription factors such as c-Myc, androgen receptor (AR), estrogen receptor (ER), β-catenin, and so on. Expression and activity of JMJD1A in cancer cells can be regulated at transcriptional, post-transcriptional, and post-translational levels. Targeting JMJD1A may repress the oncogenic transcription factors as a potential anticancer therapy.
Insights
JMJD1A, a histone demethylase, activates gene transcription by removing repressive marks. Upregulated in cancer, targeting JMJD1A offers a potential anticancer therapy by repressing oncogenic factors.
Area of Science:
- Epigenetics
- Molecular Biology
- Cancer Biology
Background:
- JMJD1A (lysine demethylase 3A) is a Jumonji C family histone demethylase.
- It removes H3K9me1/2 marks, activating gene transcription.
- JMJD1A is crucial for spermatogenesis, metabolism, sex determination, and stem cell activity.
Purpose of the Study:
- Investigate the role of JMJD1A in cancer development and progression.
- Explore JMJD1A's epigenetic regulation of oncogenic transcription factors.
- Evaluate JMJD1A as a potential therapeutic target for cancer.
Main Methods:
- Analysis of JMJD1A expression in various cancer types.
- Investigating JMJD1A's regulation at transcriptional, post-transcriptional, and post-translational levels.
- Assessing the impact of JMJD1A on key oncogenic transcription factors (e.g., c-Myc, AR, ER, β-catenin).
Main Results:
- JMJD1A is upregulated in multiple cancers, promoting tumorigenesis and therapeutic resistance.
- JMJD1A epigenetically regulates critical transcription factors involved in cancer.
- Expression and activity of JMJD1A are controlled by multiple regulatory mechanisms in cancer cells.
Conclusions:
- JMJD1A plays a significant oncogenic role in various cancers.
- Targeting JMJD1A may offer a novel therapeutic strategy by inhibiting key cancer-driving transcription factors.
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