کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10143441 | 1646180 | 2018 | 25 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MicroRNA-1301 inhibits migration and invasion of osteosarcoma cells by targeting BCL9
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کلمات کلیدی
BCL9miRNAsPVDFHRPCCK-8qRT-PCR3′-UTR - 3'-UTR3′-untranslated region - 3'-ناحیه ترجمه نشدهOsteosarcoma - استئوسارکوماsodium dodecyl sulfate-polyacrylamide gel electrophoresis - الکتروفورز ژل دوده سولفات سدیم پلی آکریل آمیدSDS-PAGE - الکتروفورز ژل پلی آکریل آمیدInvasion - تهاجمpolyvinylidene difluoride - دی فلوئورید پلی وینیلیدینmicroRNAs - ریز آرانایcell counting kit-8 - شمارش سلول کیت 8Migration - مهاجرتquantitative real-time PCR - واکنش زنجیره ای پلیمراز واقعی در زمان واقعیHorseradish peroxidase - پراکسیداز هوررادیش
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Increasing reports demonstrated that miRNAs play a critical role in tumor development and progression. Previous studies revealed that miR-1301 was abnormally expressed in various cancers. However, its function and underlying mechanism in osteosarcoma (OS) remains unknown. In this study, miR-1301 expression was significantly down-regulated in both OS tissues and cell lines. Down-regulated miR-1301 was obviously associated with malignant clinical features and poor overall survival of OS patients. miR-1301 overexpression inhibited cell proliferation, migration and invasion. In addition, we identified BCL9 act as a direct target of miR-1301 by directly binding to its 3â²-UTR. In clinical OS tissues, miR-1301 negatively correlated BCL9 expression. BCL9 was up-regulated in OS tissues and cells. BCL9 overexpression promoted OS progression. Moreover, restoration of BCL9 expression at least partially abolished the proliferation, migration and invasion of miR-1301 on OS cells. In conclusion, our data indicated that miR-1301 inhibited cell proliferation, migration and invasion of OS by targeting BCL9, and may represent a novel potential therapeutic target and prognostic marker for OS.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 679, 30 December 2018, Pages 100-107
Journal: Gene - Volume 679, 30 December 2018, Pages 100-107
نویسندگان
Lei Wang, Kejun Hu, Yu Chao,