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J. Biol. Chem., Vol. 275, Issue 45, 35256-35263, November 10, 2000
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From the Quinidine inhibits proliferation and
promotes cellular differentiation in human breast tumor epithelial
cells. Previously we showed quinidine arrested MCF-7 cells in
G1 phase of the cell cycle and led to a
G1 to G0 transition followed by apoptotic cell death. The present experiments demonstrated that MCF-7,
MCF-7ras, T47D, MDA-MB-231, and MDA-MB-435 cells
transiently differentiate before undergoing apoptosis in response to
quinidine. The cells accumulated lipid droplets, and the cytokeratin 18 cytoskeleton was reorganized. Hyperacetylated histone H4 appeared
within 2 h of the addition of quinidine to the medium, and levels
were maximal by 24 h. Quinidine-treated MCF-7 cells showed
elevated p21WAF1, hypophosphorylation and suppression of
retinoblastoma protein, and down-regulation of cyclin D1, similar to
the cell cycle response observed with cells induced to differentiate by
histone deacetylase inhibitors, trichostatin A, and trapoxin. Quinidine
did not show evidence for direct inhibition of histone deacetylase
enzymatic activity in vitro. HDAC1 was undetectable in
MCF-7 cells 30 min after addition of quinidine to the growth medium.
The proteasome inhibitors MG-132 and lactacystin completely protected
HDAC1 from the action of quinidine. We conclude that quinidine is a
breast tumor cell differentiating agent that causes the loss of HDAC1 via a proteasomal sensitive mechanism.
Rapid Induction of Histone Hyperacetylation and Cellular
Differentiation in Human Breast Tumor Cell Lines following Degradation
of Histone Deacetylase-1*
,,,¶
Department of Pharmacology & Toxicology,
Robert C. Byrd Health Sciences Center, West Virginia University,
Morgantown, West Virginia 26506 and § Manitoba Institute
of Cell Biology, University of Manitoba,
Winnipeg R3E 0V9, Canada
*
This work was supported by West Virginia University School
of Medicine, the Spurlock Cancer Research Fund, the Susan G. Komen Breast Cancer Foundation, Grants DAMD 17-99-1-9447 and DAMD
17-00-1-0500, and the Medical Research Council of Canada Grant MT-9186.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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