JMJD1A

Official Full Name

lysine demethylase 3A

Organism

Homo sapiens

GeneID

55818

Background

Enables histone H3K9me/H3K9me2 demethylase activity; iron ion binding activity; and nuclear androgen receptor binding activity. Involved in androgen receptor signaling pathway; formaldehyde biosynthetic process; and positive regulation of DNA-templated transcription. Located in nucleoplasm. Implicated in cervical cancer and colon cancer. Biomarker of Ewing sarcoma; hepatocellular carcinoma; nasopharynx carcinoma; and prostate cancer. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

KDM3A; TSGA; JMJD1; JHDM2A; JHMD2A; JMJD1A;

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Detailed Information

Recent Research

JMJD1A (Jumonji domain containing 1A, also referred to as KDM3A or JHDM2A), a member of the Jumonji C-domain containing histone demethylase family, catalyses removal of H3K9 mono- and di-methylation (H3K9me1 and H3K9me2) and functions as a co-activator for androgen receptor, as well as a crucial regulator in spermatogenesis, germ cell development, sex determination, tumorigenesis and hypoxiainducing factor-1a-mediated gene transcription. Moreover, JMJD1A regulates b-adrenergic-induced systemic metabolism and body weight control. JMJD1A deficiency results in obesity with defects in brown adipose tissue functions that lead to cold intolerance and decreased oxygen consumption. JMJD1A is a signal-sensing scaffold that regulates acute chromatin dynamics via SWI/SNF association for thermogenesis.

JMJD1A positively regulates transcription of many target genes, including YAP/TAZ (WWTR1). Furthermore, loss of JMJD1A decreases gene expression and increases the inhibitory H3K9me2 modifications in the promoter regions of multiple genes. JMJD1A was downregulated in cancer cells following detachment from CDM both on the protein and on mRNA levels. JMJD1A is downregulated following CDM exposure of cells and is a potent regulator of cancer cell proliferation in vitro and in vivo. Up-regulation of JMJD1A expression was significantly associated with infiltration depth, lymph node metastasis status, and TNM staging and cancer development, such as renal cell carcinoma and hepatocellular carcinoma. High JMJD1A expression is associated with poor clinical outcomes in human gastric cancer. Knockout of JMJD1A expression inhibits proliferation of gastric cancer cells, and further studies indicate that JMJD1A knockdown inhibits the expression of the long non-coding RNA MALAT1 by down-regulating MAPK pathway. JMJD1A acts as a scaffold that mediates distal chromatin interactions such that the distal enhancer is located near the target gene promoter of the key thermogenic gene. JMJD1A activity promotes the recruitment of androgen receptor (AR) to the c-Myc gene enhancer and induces H3K9 demethylation, increasing AR-dependent transcription of c-Myc mRNA. JMJD1A knockdown antagonizes tumorigenesis of prostate cancer cells. JMJD1A increases c-Myc protein levels by inhibiting HUWE1-induced degradation.

CDM-induced regulation of JMJD1A localization and levels is similar to the previously established regulation of YAP/TAZ. JMJD1A nuclear localization is unlikely to be dependent on a specific integrin heterodimer. JMJD1A regulates YAP/TAZ on the transcriptional level. JMJD1A and YAP/TAZ expression correlates in human cancer. JMJD1A regulates YAP/TAZ expression. JMJD1A was found to be upregulated in gastric cancer tissues and cell lines. JMJD1A was also shown to be an independent prognostic predictor of overall survival for patients with gastric cancer. JMJD1A-MALAT1-MAPK signaling might participate in the JMJD1A-induced cell proliferation of gastric cancer. JMJD1A has two important roles in regulating hormone-stimulated chromatin dynamics that modulate thermogenesis in BATs. In one role, JMJD1A is recruited to target sites and functions as a cAMP-responsive scaffold that facilitates long-range chromatin interactions, and in the second role, JMJD1A demethylates H3K9 di-methylation. JMJD1A-dependent genes function in cellular growth, proliferation and survival, and implicated that the c-Myc transcriptional network is de-regulated following JMJD1A inhibition. JMJD1A is shown to play a tumor-promoting role in several types of cancer cells such as colon carcinoma,neuroblastoma, hepatocellular carcinoma, and sarcoma.

References:

Kaukonen R, et al. Normal stroma suppresses cancer cell proliferation via mechanosensitive regulation of JMJD1a-mediated transcription. Nature Communications, 2016, 7:12237.
Yang H, et al. Elevated JMJD1A is a novel predictor for prognosis and a potential therapeutic target for gastric cancer. International Journal of Clinical & Experimental Pathology, 2015, 8(9):11092-9.
Abe Y, et al. JMJD1A is a signal-sensing scaffold that regulates acute chromatin dynamics via SWI/SNF association for thermogenesis. Nature Communications, 2015, 6:7052.
Krieg A J, et al. Regulation of the Histone Demethylase JMJD1A by Hypoxia-Inducible Factor 1α Enhances Hypoxic Gene Expression and Tumor Growth. Molecular & Cellular Biology, 2010, 30(1):344-53.

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