کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2027585 | 1542696 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dynamic monitoring of GPER-mediated estrogenic effects in breast cancer associated fibroblasts: An alternative role of estrogen in mammary carcinoma development
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کلمات کلیدی
CAFsGPCREC50ERKFAPNFsSERMFBSPBSGPERRTCAα-SMACAFnormal fibroblastsEGFRconcentration for 50% of maximal effectECM17-β-estradiol - 17 بتا استرادیولCa2+ - Ca2 +G-protein coupled receptor - G-پروتئین همراه گیرندهEstrogenic effects - اثرات استروژنα-smooth muscle actin - اکتین عضله آلفا صافBreast cancer - سرطان پستانfetal bovine serum - سرم جنین گاوPhosphate buffered saline - فسفات بافر شورcancer associated fibroblast - فیبروبلاست وابسته به سرطانExtracellular matrix - ماتریکس خارج سلولیSelective estrogen receptor modulator - مدولاتور گیرنده استروژن انتخابیTumor microenvironment - میکرو محیط زیست تومورCalcium - کلسیمextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیEstrogen receptor - گیرنده استروژنEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Cancer associated fibroblasts (CAFs) are crucial contributors to breast cancer development. Estrogen affects mammary stroma in both physiological and pathophysiological conditions. We show here that estrogen (G-protein coupled) receptor (GPER) could be detected by immunohistochemistry in stromal fibroblasts of primary breast cancers. The presence of GPER expression was further confirmed by immunofluorescence and quantitative PCR in CAFs isolated from primary breast cancers. Based on dynamic monitoring by real time cell analyzer (RTCA) system, 17-β-estradiol (E2) as well as GPER specific agonist G1 were observed to trigger transient cell index increasing within an hour in a dosage-dependent manner in breast CAFs. In addition, E2 and G1 stimulated intracellular calcium modulation and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 within seconds and minutes in CAFs, respectively. Moreover, E2 and G1 promoted cell proliferation of breast CAFs measured by RTCA monitoring, cell viability assay and cell cycle analysis, and this promotion could be blocked by a GPER-selective antagonist G15. Interestingly, dynamic RTCA monitoring indicated that E2 increased adhesion of resuspended cells, and microscopy confirmed that E2 stimulated cell spreading. Both the adhesion and spreading were proposed to be mediated by GPER, since G1 also stimulated these effects similar to E2, and G15 reduced them. Moreover, GPER was found to mediate migration that was increased by E2 and G1 but reduced by G15 in RTCA cell migration assay and transwell assay. Accordingly, GPER mediates not only rapid actions but also slow effects including adhesion/spreading, proliferation and migration in breast CAFs. Estrogen is likely to affect tumor associated stroma and contributes to mammary carcinoma development through CAFs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Steroids - Volume 112, August 2016, Pages 1-11
Journal: Steroids - Volume 112, August 2016, Pages 1-11
نویسندگان
Haojun Luo, Manran Liu, Shujuan Luo, Tenghua Yu, Chengyi Wu, Guanglun Yang, Gang Tu,