کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5589183 | 1569808 | 2017 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
microRNA-143 acts as a suppressor of hemangioma growth by targeting Bcl-2
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کلمات کلیدی
CDK5-bromo-2′-deoxy-uridineMicroRNA-143VEGFR1Endothelial Basal Medium-2EBM-2PARPRIPAqRT-PCRFBSBcl-23-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyltetrazolium bromideMTT - MTTBrdU - بروموداکسی اوریدینmiR-143 - به miR-143Proliferation - ترویجApoptosis - خزان یاختهایfetal bovine serum - سرم جنین گاوradioimmunoprecipitation assay - سنجش radioimmunoprecipitationUTR یا untranslated regions - منطقه ترجمه نشدهuntranslated region - منطقه غیر ترجمهHemangioma - همانژیومquantitative real-time polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی استPropidium iodide - پروتئین یدیدpoly (ADP-ribose) polymerase - پلی (ADP-ribose) پلیمرازcyclin-dependent kinase - کییناز وابسته به سیکلین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Infantile hemangioma is the most common vascular tumor affecting infants, which is associated with clonal expansion of endothelial cells. The aim of this study is to determine the role of microRNA (miR)-143 in the growth and survival of hemangioma-derived endothelial cells (HemECs). We examined the expression of miR-143 in patients with proliferating-phase (n = 10) and involuting-phase (n = 8) hemangiomas. The effects of ectopic expression of miR-143 on the viability, proliferation, cell cycle distribution, and apoptosis of HemECs were explored. We also identified the target gene(s) that was involved in the activity of miR-143. It was found that proliferating hemangiomas had significantly (P < 0.05) lower levels of miR-143 than involuting counterparts. Reexpression of miR-143 significantly reduced the viability and proliferation of HemECs, while knockdown of miR-143 led to an increase in the proliferation of HemECs. Moreover, overexpression of miR-143 arrested HemECs at the G0/G1 phase and promoted caspase-3-dependent apoptosis. At the molecular level, miR-143 overexpression significantly promoted the expression of p21 and p53 and reduced the expression of cyclin D1, CDK2, CDK4, and Bcl-2. Silencing of Bcl-2 phenocopied the effect of miR-143 overexpression on the proliferation and apoptosis of HemECs. Furthermore, co-expression of Bcl-2 reversed the growth-suppressive effect of miR-143 on HemECs. Taken together, miR-143 acts as a suppressor in the growth of HemECs, at least partially, through downregulation of Bcl-2. Reexpression of miR-143 may represent a potential therapeutic strategy for the treatment of proliferating hemangiomas.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 628, 10 September 2017, Pages 211-217
Journal: Gene - Volume 628, 10 September 2017, Pages 211-217
نویسندگان
Chongqing Huang, JingYong Huang, Pengyan Ma, Guanfeng Yu,