کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1963827 | 1058510 | 2011 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CK2 inhibition induces apoptosis via the ER stress response
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کلمات کلیدی
PARPTBB4,5,6,7-tetrabromobenzotriazoleC/EBP-homologous protein - C / EBP-homologous proteinPCA - PCAER stress - استرس استCHOP - تکه کردنApoptosis - خزان یاختهایProstate cancer - سرطان پروستاتendoplasmic reticulum - شبکه آندوپلاسمی Protein kinase - پروتئین کینازpoly-ADP-ribose polymerase - پلی-ADP-ریبوز پلیمرازAndrogen Receptor - گیرنده آندروژنی
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
Protein kinase CK2 is a ubiquitously expressed serine/threonine kinase consisting of two catalytic α/αⲠand two regulatory β subunits. Expression of CK2 is highly elevated in tumor cells where it protects cells from apoptosis. Accordingly inhibition of CK2 is known to induce programmed cell death, making it a promising target for cancer therapy. In the present study we investigated apoptosis induction by the CK2 inhibitor 4,5,6,7-tetrabromobenzotriazole (TBB) in prostate tumor cells. In contrast to PC-3 cells LNCaP cells respond to CK2 inhibition with apoptosis. Most interestingly we found the mitochondrial pathway induced in LNCaP as well as in PC-3 cells as monitored by down-regulation of bcl-2 and subsequent cytochrome c release. In both cell lines activation of caspase 9 was not detected. Instead, an activation of the endoplasmic reticulum (ER) stress response in LNCaP cells after treatment with the CK2 inhibitor TBB was found. We show that this ER stress response led to an up-regulation of the death receptor DR5 and subsequent apoptosis in LNCaP cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 23, Issue 1, January 2011, Pages 145-151
Journal: Cellular Signalling - Volume 23, Issue 1, January 2011, Pages 145-151
نویسندگان
Andrea Hessenauer, Carolin C. Schneider, Claudia Götz, Mathias Montenarh,