KDM3B

Official Full Name

lysine demethylase 3B

Organism

Homo sapiens

GeneID

51780

Background

Predicted to enable chromatin DNA binding activity; histone H3K9 demethylase activity; and transcription coregulator activity. Predicted to be involved in regulation of transcription by RNA polymerase II. Located in nucleoplasm. Biomarker of acute lymphoblastic leukemia; breast cancer; colorectal cancer; and lung non-small cell carcinoma. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

5qNCA; DIJOS; NET22; C5orf7; JMJD1B;

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Detailed Information

Recent Research

KDM3B is a protein containing the Jumonji C domain that enables the demethylation of monomethylated and dimethylated lysine 9 of histones H3 (H3K9me1 and H3K9me2). Its gene is located in the human 5q31 chromosomal region and is often found to be absent in breast and myeloid leukemia. KDM3B was first reported as an inhibitor of hematopoietic malignancies, so overexpression of KDM3B can inhibit tumor growth. There suggest that the loss of KDM3B may be related to the occurrence of these malignant tumors and may play a potential role in tumor inhibition. KDM3B is also associated with reproduction and cell proliferation.

KDM3B triggers the effective delay of cell proliferation by the KO of KDM3B in HepG2 cells (liver hepatocellular cells). The histone demethylase KDM3B regulates the cell cycle gene expression network of HepG2 cells in hepatoma cells. KDM3B is up-regulated in human hepatocarcinoma and that the knockout (KO) of KDM3B reduces cell proliferation by delaying the cell cycle due to the malformation of mitotic spindles. Furthermore, the cell cycle protein Cyclin D1 and proliferation factor CDC123 were significantly down-regulated in KDM3B KO cells.

KDM3B has a role in angiogenesis. KDM3B represses transcription of the angiogenesis regulatory gene, ANGPT1. Negative regulation of ANGPT1 by KDM3B is independent of its Jumonji (JmjC) domain-mediated H3K9 demethylase activity. KDM3B negatively regulates ANGPT1 transcription with its corepressor, SMRT, via recruitment to the ANGPT1 promoter. This activity is independent of its demethylase activity, suggesting that KDM3B has a mechanism by which to repress transcription of the target gene ANGPT1 to inhibit cellular proliferation and migration.

KDM3B is necessary for normal spermatogenesis and male sex. KDM3B protein was highly expressed in various cell types of mouse testis, including mesenchymal cells, supporting cells, spermatogonial cells and spermatogonial cells at different stages of differentiation. KDM3B protein is also in the epithelial cells of the caput epididymis, prostate and seminal vesicle. KDM3B KO male mice produced 44% fewer number of mature sperm in their cauda epididymides, displaying significantly reduced sperm motility. Circulation levels of 17 -estradiol, the modulator of sperm maturation and male sexual behavior, decreased significantly in KDM3B KO male mice. Notably, in male mice, the removal of KDM3B significantly increased the delay of mounts, pull-in ejaculation, and ejaculation, and decreased the number of mounts and pull-in ejaculation, mainly because they lost interest in female odor. The decreased expression level of insulin growth factor-binding protein-3 (igfbp-3) in KDM3B KO mice resulted in significantly decreased stability of igf-1 (insulin-like growth factor-1) in blood circulation, which restricted the growth of somatic cells after birth. KDM3B KO female mice were infertile because of irregular estrous cycles and decreased ovulation, fertilization, and uterine decidual response.

KDM3B-mediated H3K9 demethylation plays essential roles in maintenance of the circulating IGF-1, postnatal somatic growth, circulating 17beta-estradiol, and female reproductive function. KDM3B is a key H3K9 demethylase essential for postnatal somatic growth and female reproductive function. Disruption of KDM3B function decreases IGFBP-3 (Insulin-like growth factor-binding protein 3) expression, which results in fast degradation of IGF-1 and small body size. The loss of KDM3B function also prolongs female estrous cycle, and decreases ovulation capacity, oocyte fertilization rate, embryo implantation, decidual response and embryo growth. Together, these defects in reproductive function result in a female infertile phenotype. These defects are associated with extensive alterations of H3K9me1, H3K9me2 and/or H3K9me3 levels in the ovarian and uterine cells where Kdm3 is highly expressed.

References:

Liu Z , et al. The Histone H3K9 Demethylase Kdm3b Is Required for Somatic Growth and Female Reproductive Function. International Journal of Biological Sciences, 2015, 11(5):494-507.
Han A , et al. Transcriptional repression of ANGPT1 by histone H3K9 demethylase KDM3B. Bmb Reports, 2015, 48(7):401-406.
Liu Z , et al. Knockout of the Histone Demethylase Kdm3b Decreases Spermatogenesis and Impairs Male Sexual Behaviors. International Journal of Biological Sciences, 2015, 11(12):1447-1457.
An M J , et al. Histone demethylase KDM3B regulates the transcriptional network of cell-cycle genes in hepatocarcinoma HepG2 cells. Biochem Biophys Res Commun.:576-582.

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