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|標題:||Apoptotic and anti-proliferative effects of 17 beta-estradiol and 17 beta-estradiol-like compounds in the Hep3B cell line||作者:||Huang, E.J.
|關鍵字:||hepatocellular carcinoma (HCC);17 beta-estrodiol;17;beta-estrodiol-like compounds;apoptotic and antiproliferative effects;hepatocellular-carcinoma;postmenopausal women;sex-hormones;estrogen;liver;cancer;cirrhosis;estradiol;disease;acid||Project:||Molecular and Cellular Biochemistry||期刊/報告no：:||Molecular and Cellular Biochemistry, Volume 290, Issue 1-2, Page(s) 1-7.||摘要:||
Since there is evidence for estrogen and estrogen-like compounds to have beneficial effect on the pathogenesis of hepatocellular carcinoma (HCC), this study was designed to investigative the apoptotic and anti-proliferative effects of these compounds on the human hepatoma Hep3B cell line. The Hep3B cells were treated with 17 beta-estradiol (E2), diethylstilbestrol (DES), tamoxifen, and genistein. After treatments of these compounds at the concentration of 10(-6) or 10(-8) M, the Hep3B cells were demonstrated to have significant DNA fragmentation, nucleus condensation, cytochrome-c leaking from the mitochondria and caspase-3 activation by DAPI and Western blotting. The cells were also observed to have declined proliferative potential by MTT assay, arrested cell cycle by flow-cytometry measurements. However, the cytochrome-c leaking from the mitochondria induced by E2 and E2-like compounds was blocked totally by ICI 182,780 treatment. These finding suggest that estrogen and the estrogen-like compounds may induce anti-proliferative and apoptotic effects in Hep3B cells, and the E2 and the E2-like compounds mediated apoptotic effect was estrogen receptor dependent. Among the drugs tested, E2, E2 agonists (DES and genistein) and partial antagonist (tamoxifen), all showed the stronger anti-tumor potential.
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