کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1946343 | 1054216 | 2016 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Knockdown of long non-coding RNA MALAT1 increases the blood-tumor barrier permeability by up-regulating miR-140
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کلمات کلیدی
TEERRNA-binding protein immunoprecipitationGECsNFYmiR-140BTBLGGHGGmiRNAsncRNAslncRNAsGBMHEKqRT-PCRLCMECs - EC هاLong non-coding RNAs - RNA های بدون کدگذاری طولانیcompeting endogenous RNAs - RNA های درونزا را رقابت می کنندnon-coding RNAs - RNA های غیر کدگذاریchromatin immunoprecipitation - ایمن سازی کروماتینRISC - خطرCNS - دستگاه عصبی مرکزیmetastasis associated lung adenocarcinoma transcript 1 - رونوشت آدنوکارسینوم ریه متاستاز 1microRNAs - ریز آرانایBBB - سد خونی مغزیBlood–brain barrier - سد خونی مغزیceRNAs - سرنcentral nervous system - سیستم عصبی مرکزیzonula occludens - شل بستنNuclear factor Y - عامل هسته ای Ylaser capture microdissection - لیزر ضبط میکرو دیسکسیونMALAT1 - مالتا 1Blood–tumor barrier - مانع خون تومورRNA Induced Silencing Complex - مجتمع خاموش کننده RNA منجر شده استquantitative real-time PCR - واکنش زنجیره ای پلیمراز واقعی در زمان واقعیRIP - پاره کردنCHiP - چیپhuman embryonic kidney - کلیه جنین انسانGlioblastoma multiforme - گلیوبلاستوم مولتیفرم، گلیوبلاستوما
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The blood-tumor barrier (BTB) forms a major obstacle in brain tumor therapy by preventing the delivery of sufficient quantities of therapeutic drugs. Long non-coding RNAs (lncRNAs) play important roles in both normal development and diseases including cancer. Here, we elucidated the expression of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and defined its functional role in the regulation of BTB function as well as its possible molecular mechanisms. Our results proved that MALAT1 expression was up-regulated in brain microvessels of human glioma and glioma endothelial cells (GECs) which were obtained by co-culturing endothelial cells with glioma cells. Functionally, knockdown of MALAT1 resulted in an impairment and increased the permeability of BTB as well as decreased the expression of ZO-1, occludin and claudin-5 in GECs. Further, there was reciprocal repression between MALAT1 and miR-140, and miR-140 mediated the effects that MALAT1 knockdown exerted. Mechanistic investigations defined that nuclear factor YA (NFYA), a CCAAT box-binding transcription factor, was a direct and functional downstream target of miR-140, which was involved in the MALAT1 knockdown induced regulation of BTB function. Furthermore, NFYA could up-regulate the promoter activities and bind to the promoters of ZO-1, occludin and claudin-5 in GECs. Taken together, we have demonstrated the fact that knockdown of MALAT1 resulted in the increased permeability of BTB, which might contribute to establishing potential therapeutic strategies for human gliomas.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms - Volume 1859, Issue 2, February 2016, Pages 324-338
Journal: Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms - Volume 1859, Issue 2, February 2016, Pages 324-338
نویسندگان
Jun Ma, Ping Wang, Yilong Yao, Yunhui Liu, Zhen Li, Xiaobai Liu, Zhiqing Li, Xihe Zhao, Zhuo Xi, Hao Teng, Jing Liu, Yixue Xue,