کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8949725 | 1645722 | 2018 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Treatment-damaged hepatocellular carcinoma promotes activities of hepatic stellate cells and fibrosis through GDF15
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
GDF15HSCsTACETGFBMP7ERKFBSJnkDMEMα-SMABSA - BSAc-Jun N-terminal kinase - C-Jun N-terminal kinasetransarterial chemoembolization - chemoembolization transarterialHCC - HCCMAPK - MAPKDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده DulbeccoMitogen activated protein kinases - Mitogen فعال پروتئین کینازbovine serum albumin - آلبومین سرم گاوAlpha-smooth muscle actin - آکتا عضله آلفا صافtransforming growth factor - تبدیل فاکتور رشدfetal bovine serum - سرم جنین گاوHepatic stellate cells - سلولهای ستارهای کبدیGrowth differentiation factor 15 - عامل تمایز رشد 15Fibrosis - فیبروز یا فساد الیافMetformin - متفورمینBone morphogenetic protein-7 - پروتئین مورفوژنیک استخوان 7extracellular regulated protein kinases - پروتئین کیناز تنظیم شده خارج سلولیHepatocellular carcinoma - کارسینوم هپاتوسلولار(کارسینوم سلولهای استخوانی)
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The aim of this study was to investigate whether treatment-damaged hepatocellular carcinoma (HCC) would accelerate liver cirrhosis through promoting the activities of hepatic stellate cells (HSCs). HCC cells were exposed to chemotherapeutic agent or hypoxia to mimic the transarterial chemoembolization (TACE)-like treatment. Growth differentiation factor 15 (GDF15) expression was increased in cisplatin- or hypoxia-treated HCC cells. Treatment-induced GDF15 increase in HCC cells was mediated by p38MAPK, JNK, ERK1/2 activation. GDF15 from treatment-damaged HCC cells enhanced the proliferation and collagen synthesis of HSCs through ERK1/2- and Smad3-dependent pathways. Metformin significantly reduced the GDF15 production from treatment-damaged HCC cells by targeting JNK. The use of metformin could attenuate the in vivo fibrotic activities of HSCs promoted by treatment-damaged HCC cells and inhibit GDF15 expression. In conclusion, treatment-damaged HCC accelerates fibrosis by promoting the activities of HSCs via GDF15 secretion, which could be reversed by metformin. This provides a potential therapeutic target for alleviating TACE-aggravated liver cirrhosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 370, Issue 2, 15 September 2018, Pages 468-477
Journal: Experimental Cell Research - Volume 370, Issue 2, 15 September 2018, Pages 468-477
نویسندگان
Gang Dong, Min Ma, Xiahui Lin, Huahua Liu, Dongmei Gao, Jiefeng Cui, Zhenggang Ren, Rongxin Chen,