Abstract
Histone methylation is one of the most important chromatin posttranslational modifications. It has a range of influences on nuclear functions including epigenetic inheritance, transcriptional regulation and the maintenance of genome integrity. Changes in histone methylation status take part in various physiological and pathological processes. KDM5B (lysine demethylase 5B, also called JARID1B or PLU-1) encodes the histone H3 lysine4 (H3K4) demethylase and exhibits a strong transcriptional repression activity. KDM5B plays a role in cell differentiation, stem cell self-renewal and other developmental progresses. Recent studies showed that KDM5B expression was increased in breast, bladder, lung, prostate and many other tumors and promotes tumor initiation, invasion and metastasis. Given its association with tumor progression and prognosis of cancer patients, KDM5B was proposed to be a novel target for the prevention and treatment of human cancers. In this review, we will summarize recent advances in our understanding of the regulation and function of KDM5B in development and cancer.
Highlights
Through the modulation of chromatin structure, histone post-translational modifications including methylation, acetylation, phosphorylation and ubiquitination play a significant role in creating transcriptional activation or repression patterns [1]
KDM5B was initially identified as a gene that was up-regulated by the tyrosine kinase HER2 in human breast cancer cells and its expression was shown to be closely associated with the malignant phenotype in breast cancer [18, 25]
A newly published study demonstrated a strong increase in the expression of KDM5B in high-risk B-cell precursor acute lymphoblastic leukemia (B-ALL) compared with normal bone marrow. They found out the Ikaros DNA-binding zinc finger protein could mediate the repression of KDM5B in a manner depending on the activity of the histone deacetylase HDAC1, and this could be impaired by pro-oncogenic casein kinase 2 (CK2) [86]
Summary
Through the modulation of chromatin structure, histone post-translational modifications including methylation, acetylation, phosphorylation and ubiquitination play a significant role in creating transcriptional activation or repression patterns [1]. Another study showed that PHD1 help KDM5B target downstream genes to mediate demethylation and exert tumor-suppressor functions [23]. KDM5B was initially identified as a gene that was up-regulated by the tyrosine kinase HER2 in human breast cancer cells and its expression was shown to be closely associated with the malignant phenotype in breast cancer [18, 25].
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