کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10748932 | 1050284 | 2016 | 32 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Senescence from glioma stem cell differentiation promotes tumor growth
ترجمه فارسی عنوان
از بین رفتن سلول های بنیادی گلیوما، رشد تومور را افزایش می دهد
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کلمات کلیدی
گلیوبلاستوما، سلول بنیادی سرطانی، زناشویی، آنژیوژنز، اثر پاراکرین،
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
Glioblastoma (GBM) is a lethal brain tumor composed of heterogeneous cellular populations including glioma stem cells (GSCs) and differentiated non-stem glioma cells (NSGCs). While GSCs are involved in tumor initiation and propagation, NSGCs' role remains elusive. Here, we demonstrate that NSGCs undergo senescence and secrete pro-angiogenic proteins, boosting the GSC-derived tumor formation in vivo. We used a GSC model that maintains stemness in neurospheres, but loses the stemness and differentiates into NSGCs upon serum stimulation. These NSGCs downregulated telomerase, shortened telomeres, and eventually became senescent. The senescent NSGCs released pro-angiogenic proteins, including vascular endothelial growth factors and senescence-associated interleukins, such as IL-6 and IL-8. Conditioned medium from senescent NSGCs promoted proliferation of brain microvascular endothelial cells, and mixed implantation of GSCs and senescent NSGCs into mice enhanced the tumorigenic potential of GSCs. The senescent NSGCs seem to be clinically relevant, because both clinical samples and xenografts of GBM contained tumor cells that expressed the senescence markers. Our data suggest that senescent NSGCs promote malignant progression of GBM in part via paracrine effects of the secreted proteins.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 470, Issue 2, 5 February 2016, Pages 275-281
Journal: Biochemical and Biophysical Research Communications - Volume 470, Issue 2, 5 February 2016, Pages 275-281
نویسندگان
Rie Ouchi, Sachiko Okabe, Toshiro Migita, Ichiro Nakano, Hiroyuki Seimiya,