کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10758173 | 1050405 | 2013 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
miR-143 decreases COX-2 mRNA stability and expression in pancreatic cancer cells
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کلمات کلیدی
pKaMicroRNA-143PaCaPGE2COX-2CREB3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyltetrazolium bromideMAPK - MAPKMAPK kinase - MAPK کینازMTT - MTTmiR-143 - به miR-143Pancreatic cancer - سرطان پانکراسCyclooxygenase-2 - سیکلوکوکسیژناز2MEK - مجاهدین خلقcyclic AMP responsive element binding protein - پروتئین اتصال دهنده عنصر پاسخ دهنده AMP cyclicprotein kinase A - پروتئین کیناز Amitogen-activated protein kinase - پروتئین کیناز فعال با mitogenProstaglandin E2 - پروستاگلاندین E2
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: miR-143 decreases COX-2 mRNA stability and expression in pancreatic cancer cells miR-143 decreases COX-2 mRNA stability and expression in pancreatic cancer cells](/preview/png/10758173.png)
چکیده انگلیسی
Small non-coding RNAs, microRNAs (miRNA), inhibit the translation or accelerate the degradation of message RNA (mRNA) by targeting the 3â²-untranslated region (3â²-UTR) in regulating growth and survival through gene suppression. Deregulated miRNA expression contributes to disease progression in several cancers types, including pancreatic cancers (PaCa). PaCa tissues and cells exhibit decreased miRNA, elevated cyclooxygenase (COX)-2 and increased prostaglandin E2 (PGE2) resulting in increased cancer growth and metastases. Human PaCa cell lines were used to demonstrate that restoration of miRNA-143 (miR-143) regulates COX-2 and inhibits cell proliferation. miR-143 were detected at fold levels of 0.41 ± 0.06 in AsPC-1, 0.20 ± 0.05 in Capan-2 and 0.10 ± 0.02 in MIA PaCa-2. miR-143 was not detected in BxPC-3, HPAF-II and Panc-1 which correlated with elevated mitogen-activated kinase (MAPK) and MAPK kinase (MEK) activation. Treatment with 10 μM of MEK inhibitor U0126 or PD98059 increased miR-143, respectively, by 187 ± 18 and 152 ± 26-fold in BxPC-3 and 182 ± 7 and 136 ± 9-fold in HPAF-II. miR-143 transfection diminished COX-2 mRNA stability at 60 min by 2.6 ± 0.3-fold in BxPC-3 and 2.5 ± 0.2-fold in HPAF-II. COX-2 expression and cellular proliferation in BxPC-3 and HPAF-II inversely correlated with increasing miR-143. PGE2 levels decreased by 39.3 ± 5.0% in BxPC-3 and 48.0 ± 3.0% in HPAF-II transfected with miR-143. Restoration of miR-143 in PaCa cells suppressed of COX-2, PGE2, cellular proliferation and MEK/MAPK activation, implicating this pathway in regulating miR-143 expression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 439, Issue 1, 13 September 2013, Pages 6-11
Journal: Biochemical and Biophysical Research Communications - Volume 439, Issue 1, 13 September 2013, Pages 6-11
نویسندگان
Hung Pham, C. Ekaterina Rodriguez, Graham W. Donald, Kathleen M. Hertzer, Xiaoman S. Jung, Hui-Hua Chang, Aune Moro, Howard A. Reber, O. Joe Hines, Guido Eibl,