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Decreased expression of Cdc25a in breast stroma of diethylstilbestrol treated female ACI rats
Author(s) -
Taylor LaShaundra,
Newell Oneil,
DarlingReed Selina,
Soliman Karam,
Hudson Alicia,
Elie Yasmeen
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.lb497
Subject(s) - cdc25a , diethylstilbestrol , stroma , breast cancer , carcinogenesis , cell growth , cancer , cell cycle , estrogen , medicine , andrology , endocrinology , cancer research , biology , chemistry , immunohistochemistry , cell cycle checkpoint , biochemistry
Diethylstilbestrol (DES), a known human carcinogen and synthetic nonsteroidal estrogen has been shown to cause pituitary, breast and cervix cancers. DES has been shown to produce mammary tumors and double strand breaks in rats and induce breast cancer in humans. Diallyl sulfide (DAS), a garlic organosulfur compound (OSC) has been shown to inhibit chemical carcinogenesis in animals. OSCs like DAS are known to decrease proliferation of cancer cells by delaying cell cycle progression. The effect of DAS on the proliferation of stroma breast tissue by DES is not fully elucidated. This study will determine the proliferative properties of DAS in breast stroma of DES induced female ACI rats by examining Cdc25a and ATM expression. Female ACI rats were treated for 6 months with corn oil (control), 10mg/kg DES and/or .01mg/g DAS. RNA was isolated from breast tissue using trizol and converted to cDNA using Stratagene first strand cDNA synthesis reaction. Gene expression profiles were determined using Super Array pathway finder and confirmed with real time RT‐PCR. Cdc25a and ATM expression in the DES treated group is decreased significantly compared to the control group. Cdc25a shows an increase in the fold change in the DES/DAS group as compared to the control. We conclude that the decreased Cdc25a expression in the DES treated group may induce cell cycle arrest while the co‐treated group is approaching the level of the control. Funded by RCMI Grant #2G12RR03020‐24