کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5525408 | 1546679 | 2017 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Kindlin-2 in pancreatic stellate cells promotes the progression of pancreatic cancer
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
PSCsIngenuity Pathways AnalysisIPAhpf5-bromo-2′-deoxyuridine - 5-bromo-2'-deoxyuridineSmall interfering RNA - RNA تداخل کوچکsiRNA - siRNAPancreatic ductal adenocarcinoma - آدنوکارسینوم پانکراس داکتالPDAC یا pancreatic ductal adenocarcinoma - آدنوکارسینومای داکتال پانکراسsmooth muscle actin - آکنه عضله صافStroma - استروماIntegrin - اینتگرینBrdU - بروموداکسی اوریدینEMT - تکنسین فوریتهای پزشکیstandard error - خطای استانداردSMA - دبیرستانdesmoplasia - دزموپلازیconditioned media - رسانه های متعلق بهPancreatic Stellate Cells - سلول های ستون فقرات پانکراسpancreatic fibrosis - فیبروز پانکراسhigh power field - میدان قدرت بالاchronic pancreatitis - پانکراتیت مزمنoptical density - چگالی نوریEpithelial–mesenchymal transition - گذار اپیتلیال-مزانشیمی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Pancreatic stellate cells (PSCs) play a pivotal role in pancreatic fibrosis associated with pancreatic ductal adenocarcinoma (PDAC). Kindlin-2 is a focal adhesion protein that regulates the activation of integrins. This study aimed to clarify the role of kindlin-2 in PSCs in pancreatic cancer. Kindlin-2 expression in 79 resected pancreatic cancer tissues was examined by immunohistochemical staining. Kindlin-2-knockdown immortalized human PSCs were established using small interfering RNA. Pancreatic cancer cells were treated with conditioned media of PSCs, and the cell proliferation and migration were examined. SUIT-2 pancreatic cancer cells were subcutaneously injected into nude mice alone or with PSCs and the size of the tumors was monitored. Kindlin-2 expression was observed in PDAC and the peritumoral stroma. Stromal kindlin-2 expression was associated with shorter recurrence-free survival time after R0 resection. Knockdown of kindlin-2 resulted in decreased proliferation, migration, and cytokine expression in PSCs. The PSC-induced proliferation and migration of pancreatic cancer cells were suppressed by kindlin-2 knockdown in PSCs. In vivo, co-injection of PSCs increased the size of the tumors, but this effect was abolished by kindlin-2 knockdown in PSCs. In conclusion, kindlin-2 in PSCs promoted the progression of pancreatic cancer.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cancer Letters - Volume 390, 1 April 2017, Pages 103-114
Journal: Cancer Letters - Volume 390, 1 April 2017, Pages 103-114
نویسندگان
Naoki Yoshida, Atsushi Masamune, Shin Hamada, Kazuhiro Kikuta, Tetsuya Takikawa, Fuyuhiko Motoi, Michiaki Unno, Tooru Shimosegawa,