EHMT2 is a metastasis regulator in breast cancer

Biochem Biophys Res Commun. 2018 Feb 5;496(2):758-762. doi: 10.1016/j.bbrc.2018.01.074. Epub 2018 Jan 11.

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.

Keywords: Breast cancer; EHMT2; Invasion; Metastasis; Migration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Breast / metabolism
  • Breast / pathology
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Movement
  • Epigenesis, Genetic
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Histocompatibility Antigens / genetics*
  • Histone-Lysine N-Methyltransferase / genetics*
  • Humans
  • Neoplasm Invasiveness / genetics*
  • Neoplasm Invasiveness / pathology
  • Neoplasm Metastasis / genetics
  • Neoplasm Metastasis / pathology

Substances

  • Histocompatibility Antigens
  • EHMT2 protein, human
  • Histone-Lysine N-Methyltransferase