کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9892186 | 1541104 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Estrogen-induced apoptosis in a breast cancer model resistant to long-term estrogen withdrawal
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کلمات کلیدی
SERMSFsFBSSCs17β-estradiol - 17β استرادیولminimum essential medium - حداقل حداقل مورد نیازApoptosis - خزان یاختهایBCs - روند BCsBreast cancer - سرطان پستانfetal bovine serum - سرم جنین گاوbovine calf serum - سرم گوساله گوسالهATAC - فراخوانMEM - مامانestrogen deprivation - محرومیت استروژنSelective estrogen receptor modulator - مدولاتور گیرنده استروژن انتخابیAromatase inhibitor - مهار کننده آراماتازAromatase inhibitors - مهار کننده های آراماتازEstrogen receptor - گیرنده استروژنProgesterone receptor - گیرنده پروژسترون
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Estrogen suppression through the use of an aromatase inhibitor is an effective endocrine treatment option for postmenopausal breast cancer patients with estrogen receptor (ER)-positive disease, however, there are concerns that long-term estrogen deprivation will inevitably lead to resistance. To address the issue of acquired resistance to long-term estrogen deprivation our laboratory has developed an ER+/PRâ hormone-independent breast cancer cell line, MCF-7:5C which is a variant clone of wild-type MCF-7 cells. Originally, these cells were cultured in estrogen-free MEM containing 5% charcoal-stripped calf serum and were found to be resistant to both estradiol (E2) and antiestrogens. Interestingly, a completely different phenomenon was observed when MCF-7:5C cells were cultured in phenol red-free RPMI 1640 medium containing 10% charcoal-stripped fetal bovine serum (SFS). Using DNA quantitation assays, we examined the effect of E2 on the growth of MCF-7:5C cells under different media conditions. Our results showed that 10â9Â M E2 caused a dramatic 90% reduction in the growth of MCF-7:5C cells cultured in RPMI medium containing 10% SFS but did not have any significant inhibitory effects on cells cultured in MEM media. Additional experiments were performed to determine whether the medium or the serum facilitated the inhibitory effects of E2 and the results indicated that it was the serum. Annexin V and DAPI staining confirmed that the E2-induced growth inhibition of MCF-7:5C cells was due to apoptosis. We also examined the tumorigenic potential of MCF-7:5C cells by injecting 1Â ÃÂ 107Â cells/site into ovariectomized athymic mice and found that these cells, previously cultured in RPMI media, spontaneously grew into tumors in the absence of E2. Overall, these results show that low concentrations (>10â11Â M) of E2 are capable of inducing apoptosis in an aromatase resistant breast cancer cell model and that this effect is highly influenced by the medium in which the cells are grown.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 94, Issues 1â3, February 2005, Pages 131-141
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 94, Issues 1â3, February 2005, Pages 131-141
نویسندگان
J.S. Lewis, C. Osipo, K. Meeke, V.C. Jordan,