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Annexin A1 and cytostatic effects of HDAC inhibitors on breast adenocarcinoma cell line, MCF7
Author(s) -
Hirata Aiko,
Senanayake Thulani,
Woster Patrick M,
Hirata Fusao
Publication year - 2010
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.24.1_supplement.566.7
Subject(s) - cancer research , protein kinase b , annexin , kinase , mapk/erk pathway , histone deacetylase , chemistry , signal transduction , microbiology and biotechnology , biology , apoptosis , histone , biochemistry , gene
Annexin A1 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 other cancers, this protein is thought to have suppressor functions in these cancers. In accord with this interpretation, its expression was increased in breast adenocarcinoma MCF 7 cells as treated with THS 79‐12, a polyaminobenzamide histone N‐deacetylase (HDAC) Class 1 inhibitor, but much less with the nonspecific HDAC inhibitor, SAHA. The epigenetic induction of annexin A1 paralleled the inhibition of HDAC 1 but not the degree of apoptosis and caspase 3 activation. The cell growth of HDAC inhibitors paralleled the degrees of annexin A1 induction, but not of p21. Annexin A1 apparently increased EGF activated p38 MAP kinase, STAT3 kinase and Erk kinase, but decreased Akt kinase. Similar, if not same, changes were also observed by transfection of annexin A1 cDNA into MCF7 cells. (Supported in parts by a grant from The Susan G. Komen Breast Cancer Foundation)