MLL3/MLL4/COMPASS Family on Epigenetic Regulation of Enhancer Function and Cancer | Zendy

Christie C. Sze | Zendy; Ali Shilatifard | Zendy

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MLL3/MLL4/COMPASS Family on Epigenetic Regulation of Enhancer Function and Cancer

Author(s) -

Christie C. Sze,

Ali Shilatifard

Publication year - 2016

Publication title -

cold spring harbor perspectives in medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.853

H-Index - 105

eISSN - 2472-5412

pISSN - 2157-1422

DOI - 10.1101/cshperspect.a026427

Subject(s) - enhancer , demethylase , epigenetics , biology , histone , carcinogenesis , ezh2 , microbiology and biotechnology , histone h3 , histone methyltransferase , computational biology , mef2 , genetics , cancer , gene , gene expression

During development, precise spatiotemporal patterns of gene expression are coordinately controlled by cis-regulatory modules known as enhancers. Their crucial role in development helped spur numerous studies aiming to elucidate the functional properties of enhancers within their physiological and disease contexts. In recent years, the role of enhancer malfunction in tissue-specific tumorigenesis is increasingly investigated. Here, we direct our focus to two primary players in enhancer regulation and their role in cancer pathogenesis: MLL3 and MLL4, members of the COMPASS family of histone H3 lysine 4 (H3K4) methyltransferases, and their complex-specific subunit UTX, a histone H3 lysine 27 (H3K27) demethylase. We review the most recent evidence on the underlying roles of MLL3/MLL4 and UTX in cancer and highlight key outstanding questions to help drive future research and contribute to our fundamental understanding of cancer and facilitate identification of therapeutic opportunities.

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