کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10899940 | 1084434 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Modulation of the Wnt/beta-catenin pathway in human oligodendroglioma cells by Sox17 regulates proliferation and differentiation
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کلمات کلیدی
OligodendrogliomasMBPSMORT-PCRSOX17DHHPTCfrizzledFZDCNPaseIHHSFRP12′,3′-Cyclic-Nucleotide 3′-PhosphodiesteraseWntOPCs - OPC هاBrdU - بروموداکسی اوریدینHog - تیراندازیDesert Hedgehog - خارپشت بیابانIndian Hedgehog - خارپشت هندیShh - خیرOligodendrocyte progenitor cells - سلول های پیش گیاه Oligodendrocytecytomegalovirus - سیتومگالوویروسCMV - سیتومگالوویروسSmoothened - صافsonic hedgehog - صدای جیر جیرreverse transcription-polymerase chain reaction - واکنش زنجیره ای رونویسی-پلیمراز معکوسSecreted frizzled related protein - پروتئین مربوط به فروتوزاسیون ترشح می شودMyelin basic protein - پروتئین پایه میلینPatched - پچ شدهoligodendrocyte progenitor - پیشگام اولیگودندروسیتCell cycle - چرخه سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Oligodendrogliomas originate from oligodendrocyte progenitor cells (OPCs), whose development is regulated by the Sonic hedgehog and Wnt/beta-catenin pathways. We investigated the contribution of these pathways in the proliferation and differentiation of human oligodendroglioma cells (HOG). Inhibition of Hedgehog signaling with cyclopamine decreased cell survival and increased phosphorylated beta-catenin without altering myelin protein levels. Conversely, treatment of HOG with the Wnt antagonist secreted frizzled related protein (SFRP1), led to increased myelin protein levels and reduced cell proliferation, suggesting cell cycle arrest and differentiation. Unlike normal primary human OPCs, beta-catenin in HOG cells is not associated with endogenous Sox17 protein despite high levels of both proteins. Retroviral overexpression of recombinant Sox17 increased HOG cell cycle exit and apoptosis, and raised myelin protein levels and the percentage of O4+ cells, indicating increased differentiation. Recombinant Sox17 also increased beta-catenin-TCF4-Sox17 complex formation and decreased total cellular levels of beta-catenin. These changes were associated with increased SFRP1, and reduced expression of Wnt-1 and Frizzled-1, -3 and -7 RNA, indicating that Sox17 induced a Hedgehog target, and regulated Wnt signaling at multiple levels. Our studies indicate that Wnt signaling regulates HOG cell cycle arrest and differentiation, and that recombinant Sox17 mediates modulation of the Wnt pathway through changes in beta-catenin, SFRP1 and Wnt/Frizzled expression. Our results thus identify Sox17 as a potential molecular target to include in HOG therapeutic strategies.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cancer Letters - Volume 335, Issue 2, 28 July 2013, Pages 361-371
Journal: Cancer Letters - Volume 335, Issue 2, 28 July 2013, Pages 361-371
نویسندگان
Hui-Ling Chen, Li-Jin Chew, Roger J. Packer, Vittorio Gallo,