کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815155 | 1058454 | 2015 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of prostate stromal fibroblasts by the PIM1 protein kinase
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کلمات کلیدی
MyofibroblastsPDGFRαSMACAFsCOL1A1Ccl5Collagen type I alpha 1PIM1GFPTMADOXPCA - PCAsmooth muscle actin - آکنه عضله صافIHC - ایمونوهیستوشیمیImmunohistochemistry - ایمونوهیستوشیمیdoxycycline - داکسی سایکلینProstate cancer - سرطان پروستاتCancer associated fibroblasts - فیبروبلاست های مرتبط با سرطانbone marrow - مغز استخوانTissue microarray - میکروآرشی بافتBPH - هیپرپلازی خوش خیم پروستات یا BPHBenign prostate hyperplasia - هیپرپلازی پروستات خوش خیمquantitative real-time polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی استchemokine (C-C motif) ligand 5 - کیموکین (C-C motif) لیگاند 5platelet-derived growth factor receptors - گیرنده های فاکتور رشد فلوتر
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Regulation of prostate stromal fibroblasts by the PIM1 protein kinase Regulation of prostate stromal fibroblasts by the PIM1 protein kinase](/preview/png/10815155.png)
چکیده انگلیسی
The PIM1 oncogene is over-expressed in human prostate cancer epithelial cells. Importantly, we observe that in human hyperplastic and cancerous prostate glands PIM1 is also markedly elevated in prostate fibroblasts, suggesting an important role for this kinase in epithelial/stromal crosstalk. The ability of PIM1 to regulate the biologic activity of stromal cells is demonstrated by the observation that expression of PIM1 kinase in human prostate fibroblasts increases the level and secretion of the extracellular matrix molecule, collagen 1A1 (COL1A1), the pro-inflammatory chemokine CCL5, and the platelet-derived growth factor receptors (PDGFR). PIM1 is found to regulate the transcription of CCL5. In co-cultivation assays where PIM1 over-expressing fibroblasts are grown with BPH1 prostate epithelial cells, PIM1 activity markedly enhances the ability of these fibroblasts to differentiate into myofibroblasts and express known markers of cancer-associated fibroblasts (CAFs). This differentiation can be reversed by the addition of small molecule PIM kinase inhibitors. Western blots demonstrate that PIM1 expression in prostate fibroblasts stimulates the phosphorylation of molecules that regulate 5â²Cap driven protein translation, including 4EBP1 and eIF4B. Consistent with the hypothesis that the kinase controls translation of specific mRNAs in prostate fibroblasts, we demonstrate that PIM1 expression markedly increases the level of COL1A1 and PDGFRβ mRNA bound to polysomes. Together these results point on PIM1 as a novel factor in regulation of the phenotype and differentiation of fibroblasts in prostate cancer by controlling both the transcription and translation of specific mRNAs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 27, Issue 1, January 2015, Pages 135-146
Journal: Cellular Signalling - Volume 27, Issue 1, January 2015, Pages 135-146
نویسندگان
Marina Y. Zemskova, Jin H. Song, Bo Cen, Javier Cerda-Infante, Viviana P. Montecinos, Andrew S. Kraft,