Dissecting the role of the epigenetic reader TRIM33 in Multiple Myeloma
Multiple Myeloma (MM) is a haematological neoplasm characterised by the clonal proliferation of malignant plasma cells in the bone marrow. Altered epigenetic regulation of gene expression is emerging as an important player in MM pathogenesis. Through previous studies we have identified the epigenetic reader protein TRIM33 as a potential tumour suppressor gene in MM. Loss of TRIM33 is observed in approximately 20% of MM patients and is significantly associated with disease progression and reduced overall survival.
Conversely, overexpression of TRIM33 in MM cell lines inhibits proliferation. TRIM33 contains a PHD and bromodomain which bind histone 3 at trimethylated lysine 9 (H3K9me3) and acetylated lysine 18 (H3K18ac), respectively. A number of recent studies point to a role for H3K9 methylation in MM. This study aims to delineate the role of TRIM33 in H3K9 methylation and determine its functional significance in MM. TRIM33 loss-of-function and gain-of-function isogenic cell lines will be generated using CRISPR/Cas9 gene editing technology and used to characterize the epigenomic and gene expression changes associated with TRIM33 loss in MM. There is an ever growing list of epigenetic therapies that are under investigation in MM.
It is anticipated that this study will identify therapeutic vulnerabilities in MM that may be targeted by some of these agents.
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Sunday, January 20, 2019
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