ATP depletion as a consequence of hypoxia enhances tamoxifen antiproliferative effects in T47D breast carcinoma cells

Tamoxifen causes a mitochondrial transmembrane potential dysfunction and ATP depletion, which may play a role in tamoxifen cytotoxicity. Administration of oligomycin-2 deoxy glucose (2DG) enhanced tamoxifen antiproliferative effects, which may be due to exacerbated ATP depletion following tamoxifen...

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Bibliographic Details
Published inOncology research Vol. 18; no. 5-6; p. 221
Main Authors Seyedabadi, M, Ghahremani, M H, Ostad, S N
Format Journal Article
LanguageEnglish
Published United States 01.01.2009
Subjects
Adenosine Triphosphate - metabolism
Antimetabolites - pharmacology
Antineoplastic Agents, Hormonal - pharmacology
Blotting, Western
Breast Neoplasms - drug therapy
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Cell Cycle - drug effects
Cell Proliferation - drug effects
Deoxyglucose - pharmacology
Female
Flow Cytometry
Humans
Hypoxia - metabolism
Tamoxifen - pharmacology
Tumor Cells, Cultured
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Summary:Tamoxifen causes a mitochondrial transmembrane potential dysfunction and ATP depletion, which may play a role in tamoxifen cytotoxicity. Administration of oligomycin-2 deoxy glucose (2DG) enhanced tamoxifen antiproliferative effects, which may be due to exacerbated ATP depletion following tamoxifen and oligomycin-2DG coadministration. Sodium nitroprusside (SNP) did not significantly change tamoxifen responsiveness at 0.1, 0.5, and 1 mM; however, 2 mM SNP hampered tamoxifen effects on cell proliferation and cell cycle. Oligomycin-2DG neither changed iNOS expression nor altered its attenuated expression due to tamoxifen exposure, suggesting that ATP depletion-mediated sensitivity to tamoxifen seems to be apart from iNOS.
ISSN:0965-0407
1555-3906
DOI:10.3727/096504009X12596189659204