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.
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http://dx.doi.org/10.1002/mc.23390 | DOI Listing |
Cancer Genomics Proteomics
October 2024
Department of Oto-Rhino-Laryngology, Head and Neck Surgery, University Hospital Wuerzburg, Wuerzburg, Germany.
Background/aim: This study aimed to assess the impact of hypoxia on epithelial-mesenchymal transition (EMT) in head and neck squamous cell carcinoma (HNSCC), focusing on the involvement of transcription factors hypoxia inducible factor 1 (HIF-1α) and Jumonji Domain-Containing Protein 1A (JMJD1A).
Materials And Methods: FaDu and Cal33 cell lines were subjected to hypoxic and normoxic conditions. Cell proliferation was quantified electronically, while PCR and western blot analyses were used to measure mRNA and protein levels of HIF-1α, JMJD1A, and EMT markers.
Adv Exp Med Biol
September 2023
Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 655 W Baltimore Street, Baltimore, MD, USA.
Methylation of histone H3 lysine 9 (H3K9) is a repressive histone mark and associated with inhibition of gene expression. KDM3 is a subfamily of the JmjC histone demethylases. It specifically removes the mono- or di-methyl marks from H3K9 and thus contributes to activation of gene expression.
View Article and Find Full Text PDFJ Korean Med Sci
August 2023
Department of Neurosurgery, Samsung Changwon Hospital, Sungkyunkwan University School of Medicine, Changwon, Korea.
Background: This study aimed to identify the specific T cell co-stimulatory and co-inhibitory factors that play prognostic roles in patients with glioblastoma. Additionally, the unique histone H3 modification enzymes that regulate the expression levels of these specific co-stimulatory and co-inhibitory factors were investigated.
Methods: The medical records of 84 patients newly diagnosed with glioblastoma at our institution from January 2006 to December 2020 were retrospectively reviewed.
Nat Cell Biol
July 2023
Department of Molecular Genetics, Erasmus University Medical Center, Erasmus MC Cancer Institute, Rotterdam, the Netherlands.
Chromatin is dynamically reorganized when DNA replication forks are challenged. However, the process of epigenetic reorganization and its implication for fork stability is poorly understood. Here we discover a checkpoint-regulated cascade of chromatin signalling that activates the histone methyltransferase EHMT2/G9a to catalyse heterochromatin assembly at stressed replication forks.
View Article and Find Full Text PDFFront Oncol
February 2023
Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States.
BHLHE40 is a transcription factor, whose role in colorectal cancer has remained elusive. We demonstrate that the gene is upregulated in colorectal tumors. Transcription of was jointly stimulated by the DNA-binding ETV1 protein and two associated histone demethylases, JMJD1A/KDM3A and JMJD2A/KDM4A, which were shown to also form complexes on their own and whose enzymatic activity was required for upregulation.
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