کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8531222 | 1559731 | 2018 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
B7-H6 expression is induced by lipopolysaccharide and facilitates cancer invasion and metastasis in human gliomas
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کلمات کلیدی
CCK-8Bcl-2granulocyte-macrophage colony stimulating factorNKP30GAPDHPD-L1MMP-9qPCRGM-CSFFBSMMP-2DMEMLPSDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده Dulbeccoshort interfering RNA - RNA تداخل کوتاهsiRNA - siRNAinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینBax - باکسtumor necrosis factor-α - تومور نکروز عامل αEMT - تکنسین فوریتهای پزشکیfetal bovine serum - سرم جنین گاوcell counting kit-8 - شمارش سلول کیت 8Vascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)TNF-α - فاکتور نکروز توموری آلفاB-cell lymphoma-2 - لنفوم سلول B-2lipopolysaccharide - لیپوپلی ساکاریدMatrix metalloproteinase-9 - ماتریکس متالوپروتئیناز -9Matrix metalloproteinase-2 - ماتریکس متالوپروتئیناز-2programmed death-ligand 1 - مرگ برنامهریزی لیگاند 1wild-type - نوع وحشیreal-time quantitative polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی استBcl-2 Associated X protein - پروتئین Bcl-2 Associated XCancer progression - پیشرفت سرطانEpithelial-mesenchymal transition - گذار اپیتلیال-مزانشیمیglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژنازGlioma - گلیوما
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Although great progress has been made in treatment regimens, gliomas are still incurable and the 5-year survival remains poor. Studies focusing on molecules that regulate tumorigenesis or tumor immunity may provide potential therapeutic strategies for patients with glioma. B7-H6 is selectively expressed in tumor cells and plays vital roles in host immune responses. In this study, we demonstrated that B7-H6 was expressed in glioma cell lines, including CRT, U251, SHG-44, SF-295, TG-905 and U373, and tumor tissues isolated from glioma patients. Moreover, the expression levels of B7-H6 were significantly correlated with glioma grade. Previous studies reported that inflammatory mediators and cytokines induced the expression of B7 family members including programmed death-ligand 1, B7-H2 and B7-H4. Therefore, we explored the regulation of B7-H6 expression in gliomas and showed that lipopolysaccharide induced the expression of B7-H6 in glioma cells. To further analyze the roles of B7-H6 in gliomas, the expression of B7-H6 in glioma cells was knocked down. The results of cell counting kit-8, colony formation, wound healing, and transwell migration and invasion assays demonstrated that the proliferation, migration and invasion of glioma cells were inhibited after knocking down B7-H6. To elucidate the specific mechanisms of B7-H6 function in cancer progression, we examined the expression levels of proteins involved in cell apoptosis, migration and invasion. We demonstrated that the expression levels of E-cadherin and Bcl-2 associated X protein increased, and the expression levels of vimentin, N-cadherin, matrix metalloproteinase-2, matrix metalloproteinase-9 and survivin decreased after knocking down B7-H6. In conclusion, B7-H6 plays important roles in glioma, and targeting B7-H6 may provide a novel therapeutic strategy for glioma patients.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 59, June 2018, Pages 318-327
Journal: International Immunopharmacology - Volume 59, June 2018, Pages 318-327
نویسندگان
Fengyuan Che, Xiaoli Xie, Long Wang, Quanping Su, Feiyu Jia, Yufu Ye, Lanlan Zang, Jing Wang, Hongyan Li, Yanchun Quan, Cuiping You, Jiawei Yin, Zhiqiang Wang, Gen Li, Yifeng Du, Lijuan Wang,