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In JoVE (1)
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Articles by Yayesh Asmerom in JoVE
Medição bioquímicos da Hipóxia Neonatal
Megan S. Plank1, Teleka C. Calderon1, Yayesh Asmerom2, Danilo S. Boskovic1, Danilyn M. Angeles2
1Division of Biochemistry, Department of Basic Sciences, Loma Linda University, 2Division of Physiology, Department of Basic Sciences, Loma Linda University
Um método é descrito para medir marcadores bioquímicos de hipóxia-isquemia neonatal. A abordagem utiliza cromatografia líquida de alta pressão (HPLC) e Cromatografia Gasosa Espectrometria de Massa (GC / MS).
Other articles by Yayesh Asmerom on PubMed
Endocrinology. Oct, 2005 | Pubmed ID: 16037384
IGF-II is a potent mitogen and inhibitor of apoptosis in breast cancer. Regulation of IGF-II is complex and includes inhibition by tumor suppressors, stimulation by oncogenes, and imprinting and hormonal regulation by estrogens. Resveratrol (RSV) is a phytoestrogen that displays estrogen-like agonistic and antagonistic activity. Recent studies have shown that RSV inhibits the growth of breast cancer cells and may represent a potent agent in chemopreventive therapy. Because 17beta-estradiol regulates IGF-II, we hypothesized that RSV may have a similar effect on IGF-II. The present study was designed to examine whether: 1) RSV modulates IGF-II in breast cancer cells; 2) regulation of IGF-II by RSV is dependent on the ER status; and 3) IGF-II (not IGF-I) mediates RSV effects on breast cancer cells. Treatment of MCF-7 and T47D cells with RSV (10(-6) M) caused stimulation of precursor IGF-II mRNA and protein; this effect was blocked by coincubation with 17beta-estradiol (10(-9) M). Cell growth stimulated by RSV (10(-6) M) was blocked by addition of a blocking IGF-I receptor antibody, or the antiestrogen tamoxifen (10(-7) M). In contrast, RSV treatment (10(-4) M) inhibited IGF-II secretion and cell growth in MCF-7 and T47D cells. No increase in IGF-II levels is seen in estrogen receptor (-) MCF-10 cells, even though cell growth was inhibited by RSV 10(-4) M and precursor IGF-II blocked the inhibitory effect of resveratrol. No change in IGF-I was observed with RSV treatment (10(-6) to 10(-4) M). Our study demonstrates that RSV regulates IGF-II and that IGF-II mediates RSV effect on cell survival and growth in breast cancer cells.
Insulin-like Growth Factor II Mediates Resveratrol Stimulatory Effect on Cathepsin D in Breast Cancer Cells
Growth Factors (Chur, Switzerland). Mar, 2006 | Pubmed ID: 16393696
Cathepsin D (CD) is an enzyme that promotes breast cancer. CD is stored intracellularly; however, we demonstrated that IGF-II promotes CD secretion in estrogen receptor positive (ER+) breast cancer cells. We also showed that resveratrol (RSV) stimulates IGF-II in ER(+) breast cancer cells. Thus, we designed this study to determine whether RSV regulates CD in MCF-7, T47D (ER+) breast cancer cells as well as in Hs578t (cancer) and MCF-10A (normal) ER - cell lines. RSV (10(- 6) M) increased CD and IGF-II secretion in ER+ but not ER - cells. RSV treatment (10(- 4) M) inhibited CD in ER+ but not in ER - cells. Transfection of ER - cells with proIGF-II increased CD secretion. RSV (10(- 6) M) modulates CD secretion through IGF-II while RSV (10(- 4) M) inhibits CD in ER+ but not ER - cells. Regulation of CD by RSV represents a novel mechanism by which RSV may protect against breast cancer.