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For breast cancer treatment, hormone therapy is effective for hormone receptor-positive breast cancer but not for TNBC (triple-negative breast cancer). Thus, many researchers have attempted to identify more effective therapeutic candidates for all subtypes of breast cancer. In this study, we established an RNA-seq analytical pipeline to analyze the subtype-specific functions of EHMT2 in the MB231 and MCF7 cell lines. After EHMT2 knockdown, we identified subtype-specific DEGs (differentially expressed genes) and overlapping DEGs. Through GO (Gene Ontology) analysis, GSEA (gene set enrichment analysis), and KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis using the DEGs, we identified the subtype-specific functions of EHMT2 in the MB231 and MCF7 cell lines. Therefore, herein, we suggest that EHMT2 is an attractive therapeutic target for the treatment of all types of breast cancer. • EHMT2 knockdown suppressed cell proliferation and migration/invasion in MB231 and MCF7. • In RNA-seq analysis, EHMT2 have cell type specific functions in MB231 and MCF7. • EHMT2 is an attractive therapeutic target for treating all types of breast cancer. [ABSTRACT FROM AUTHOR]

Abstract Various modes of epigenetic regulation of breast cancer proliferation and metastasis have been investigated, but epigenetic mechanisms involved in breast cancer metastasis remain elusive. Thus, in this study, EHMT2 (a histone methyltransferase) was determined to be significantly overexpressed in breast cancer tissues and in Oncomine data. In addition, knockdown of EHMT2 reduced cell migration/invasion and regulated the expression of EMT-related markers (E-cadherin, Claudin 1, and Vimentin). Furthermore, treatment with BIX-01294, a specific inhibitor of EHMT2, affected migration/invasion in MDA-MB-231 cells. Therefore, our findings demonstrate functions of EHMT2 in breast cancer metastasis and suggest that targeting EHMT2 may be an effective therapeutic strategy for preventing breast cancer metastasis. Highlights • EHMT2 (a histone methyltransferase) was determined to be significantly overexpressed in breast cancer tissues. • Knockdown of EHMT2 reduced cell migration/invasion and regulated the expression of EMT-related markers. • EHMT2 regulated EMT markers via up-regulation of MSK1-SNAIL1. [ABSTRACT FROM AUTHOR]