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Epigenetic expression of annexin A1 and cytostatic effects of HDAC inhibitors in breast adenocarcinoma cell line, MCF 7
Author(s) -
Hirata Aiko,
Senanayake Thulani,
How Yingchun,
Woster Patrick W,
Hirata Fusao
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.925.1
Subject(s) - mcf 7 , cancer research , annexin , signal transduction , cell growth , transfection , biology , microbiology and biotechnology , cancer cell , annexin a2 , annexin a1 , cell culture , apoptosis , chemistry , cancer , biochemistry , genetics , human breast
Annexin A1 is a member of the protein family that binds to phospholoipids in a Ca2+ dependent manner, and from its chemical nature is thought to be closely associated with membrane functions such as membrane organization, trafficking and metabolism. On the other hand, this protein is a major substrate of oncogenic kinases such as c‐met and c‐src, and is thus proposed to be involved in signal transduction of growth factors and mitogens. Since the expression of annexin A1 is decreased in breast cancer and prostate cancer, this protein is thought to have supressor functions in these cancers. In accord with this interpretation, its expression was increased, when breast adenocarcinoma MCF 7 cells were treated with THS‐79‐12, a polyaminobenzamide histone N‐deacetylase (HDAC) Class 1 inhibitor. The epigenetic induction of annexin A1 paralleled the inhibition of HDAC. The cell growth of THS‐79‐12 treated MCF 7 cells was arrested, and their morphology became similar to that of normal breast epithelial cells, MCF 10A. The cell morphology and cell growth of MCF 7 cells transfected by cDNA encoding human annexin A1 exhibited similar changes with those of THS‐79‐12 treated cells. Roles of annexin A1 in apoptosis pathway and EGF signal transduction will be discussed. (Supported in parts by a grant from The Susan G. Komen Breast Cancer Foundation.)