Opposite effects of HDAC inhibitors on glucocorticoid and estrogen signaling in human endometrial Ishikawa cells

نویسندگان

  • Walter Rocha
  • Rocio Sanchez
  • Julie Deschênes
  • Anick Auger
  • Elise Hébert
  • John H. White
  • Sylvie Mader
چکیده

Department of Biochemistry, Université de Montréal, Montréal QC H3C 3J7 (W.R., R.S., J.D., A.A., E.H., S.M.), Institute of Research in Immunology and in Cancerology, Université de Montréal, Montréal QC H3C 3J7 (W.R., J.D., E.H., S.M.), Montreal Center for Experimental Therapeutics in Cancer, Jewish General Hospital, Montreal QC H3T 1E2 (W.R., J.D., E.H., J.H.W., S.M.), Department of Physiology, McGill University, Montréal QC H3J 1Y6 (J.H.W.), Department of Medicine, McGill University, Montréal QC H3J 1Y6 (J.H.W., S.M.). Molecular Pharmacology Fast Forward. Published on September 26, 2005 as doi:10.1124/mol.105.014514

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Opposite effects of histone deacetylase inhibitors on glucocorticoid and estrogen signaling in human endometrial Ishikawa cells.

Histone deacetylase inhibitors (HDACi), which have emerged as a new class of anticancer agents, act by modulating expression of genes controlling apoptosis or cell proliferation. Here, we compared the effect of HDACi on transcriptional activation by estrogen or glucocorticoid receptors (ER and GR, respectively), two members of the steroid receptor family with cell growth regulatory properties. ...

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Histone deacetylase (HDAC) inhibitors are a new class of anticancer agents that act by inhibiting cancer cell proliferation and inducing apoptosis both in vitro and in vivo. This study examined the anti-tumor effect of apicidin on human endometrial cancer Ishikawa cells in an animal model by inhibiting specific HDAC expression. Nude mice were injected subcutaneously (s.c.) with Ishikawa cells, ...

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تاریخ انتشار 2005