کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6074803 | 1203488 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
RanBP3 Regulates Melanoma Cell Proliferation via Selective Control of Nuclear Export
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کلمات کلیدی
nESTGF-βERKRANBP3Crm1ERK1/2 - ERK1 / 2MAPK/ERK kinase - MAPK / ERK kinaseSmall interfering RNA - RNA تداخل کوچکsiRNA - siRNABAD - بدtransforming growth factor-β - تبدیل فاکتور رشد βNuclear export sequence - توالی صادرات هسته ایMEK - مجاهدین خلقchromosome region maintenance 1 - نگهداری منطقه کروموزوم 1mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase 1/2 - کیناز 1/2 تنظیم سیگنال خارج سلولیextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
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چکیده انگلیسی
Chromosome region maintenance 1-mediated nucleocytoplasmic transport has been shown as a potential anticancer target in various malignancies. However, the role of the most characterized chromosome region maintenance 1 cofactor ran binding protein 3 (RanBP3) in cancer cell biology has never been investigated. Utilizing a loss-of-function experimental setting in a vast collection of genetically varied melanoma cell lines, we observed the requirement of RanBP3 in melanoma cell proliferation and survival. Mechanistically, we suggest the reinstatement of transforming growth factor-β (TGF-β)-Smad2/3-p21Cip1 tumor-suppressor axis as part of the RanBP3 silencing-associated antiproliferative program. Employing extensive nuclear export sequence analyses and immunofluorescence-based protein localization studies, we further present evidence suggesting the requirement of RanBP3 function for the nuclear exit of the weak nuclear export sequence-harboring extracellular signal-regulated kinase protein, although it is dispensable for general CRM1-mediated nuclear export of strong nuclear export sequence-harboring cargoes. Rendering mechanistic support to RanBP3 silencing-mediated apoptosis, consequent to extracellular signal-regulated kinase nuclear entrapment, we observed increased levels of cytoplasmically restricted nonphosphorylated/active proapoptotic Bcl-2-antagonist of cell death (BAD) protein. Last, we present evidence suggesting the frequently activated mitogen-activated protein kinase signaling in melanoma as a potential founding basis for a deregulated post-translational control of RanBP3 activity. Collectively, the presented data suggest RanBP3 as a potential target for therapeutic intervention in human melanoma.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 136, Issue 1, January 2016, Pages 264-274
Journal: Journal of Investigative Dermatology - Volume 136, Issue 1, January 2016, Pages 264-274
نویسندگان
Gaurav Pathria, Bhavuk Garg, Christine Wagner, Kanika Garg, Melanie Gschaider, Ahmad Jalili, Stephan N. Wagner,