کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5851698 | 1561786 | 2013 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Production of Cyr61 protein is modulated by extracellular acidification and PI3K/Akt signaling in prostate carcinoma PC-3 cells
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
ECMCellular FLICE-like inhibitory proteinCyr61PI3Kc-FLIPPBSSDSECLNACHRPN-acetylcysteine - N-استیل سیستئینp-Akt - P-AKTSmall interfering RNA - RNA تداخل کوچکsiRNA - siRNAAkt - آکتenhanced chemiluminescence - بهبود شیمیایی لومنsodium dodecyl sulfate - سدیم دودسیل سولفاتProstate cancer - سرطان پروستاتPhosphate buffered saline - فسفات بافر شورphosphoinositide 3-kinase - فسفینوزیتید 3-کینازExtracellular matrix - ماتریکس خارج سلولیApoptotic cell death - مرگ سلولی آپوپتوزHorseradish peroxidase - پراکسیداز هوررادیش
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش تغذیه
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Production of Cyr61 protein is modulated by extracellular acidification and PI3K/Akt signaling in prostate carcinoma PC-3 cells Production of Cyr61 protein is modulated by extracellular acidification and PI3K/Akt signaling in prostate carcinoma PC-3 cells](/preview/png/5851698.png)
چکیده انگلیسی
High expression of Cyr61, an extracellular cysteine-rich heparin-binding protein, has been associated with a malignant cell phenotype and poor outcome in prostate cancers. Although Cyr61 was found by us to be overproduced in androgen-independent PC-3 cells treated with N-acetylcysteine (NAC), its significance is still unclear. We therefore aimed to determine how and why Cyr61 protein is overexpressed in NAC-treated cells. Here, we found that Cyr61 protein level markedly increased in cells treated with NAC at high cell seeding density. Silencing of Cyr61 by siRNA induced enhanced activity of caspase-3/7, upregulation of the proapototic Bok, BimL and BimS, cleavage of apoptosis hallmarkers such as Bax, PARP and caspase-3, and downregulation of antiapoptotic Bcl2, Bcl-xL and Mcl-1 proteins. NAC treatment caused a reduction of extracellular medium pH to acidic and an increase in Akt phosphorylation, after which the replacement with NAC-free medium returned them to control levels within 24Â h. Acid stimulation increased the levels of Cyr61 and p-Akt proteins, whereas it suppressed the induction of proapoptotic and antiapoptotic proteins. Overall, our data indicate that PC-3 cells overproduce Cyr61 protein via activation of the PI3K/Akt signaling as a part of the survival mechanisms under the conditions causing extracellular acidity and further cytotoxicity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Food and Chemical Toxicology - Volume 58, August 2013, Pages 169-176
Journal: Food and Chemical Toxicology - Volume 58, August 2013, Pages 169-176
نویسندگان
Yoon-Jin Lee, David M. Lee, Sang-Han Lee,