https://scholars.lib.ntu.edu.tw/handle/123456789/458580
標題: | Insulin-like growth factors inhibit dendritic cell-mediated anti-tumor immunity through regulating ERK1/2 phosphorylation and p38 dephosphorylation | 作者: | Huang C.-T. Chang M.-C. YU-LI CHEN Chen T.-C. CHI-AN CHEN WEN-FANG CHENG |
公開日期: | 2015 | 卷: | 359 | 期: | 1 | 起(迄)頁: | 117-126 | 來源出版物: | Cancer Letters | 摘要: | Insulin-like growth factors (IGFs) can promote tumorigenesis via inhibiting the apoptosis of cancer cells. The relationship between IGFs and dendritic cell (DC)-mediated immunity were investigated. Advanced-stage ovarian carcinoma patients were first evaluated to show higher IGF-1 and IGF-2 concentrations in their ascites than early-stage patients. IGFs could suppress DCs' maturation, antigen presenting abilities, and the ability to activate antigen-specific CD8+ T cell. IGF-treated DCs also secreted higher concentrations of IL-10 and TNF-α. IGF-treated DCs showed decreased ERK1/2 phosphorylation and reduced p38 dephosphorylation. The percentages of matured DCs in the ascites were significantly lower in the IGF-1 or IGF-2 highly-expressing WF-3 tumor-bearing mice. The IGF1R inhibitor - NVP-AEW541, could block the effects of IGFs to rescue DCs' maturation and to restore DC-mediated antigen-specific immunity through enhancing ERK1/2 phosphorylation and p38 dephosphorylation. IGFs can inhibit DC-mediated anti-tumor immunity through suppressing maturation and function and the IGF1R inhibitor could restore the DC-mediated anti-tumor immunity. Blockade of IGFs could be a potential strategy for cancer immunotherapy. ? 2015 Elsevier Ireland Ltd. |
URI: | 2-s2.0-84964296335 https://scholars.lib.ntu.edu.tw/handle/123456789/458580 |
ISSN: | 0304-3835 | DOI: | 10.1016/j.canlet.2015.01.007 | SDG/關鍵字: | interleukin 10; mitogen activated protein kinase 1; mitogen activated protein kinase 3; somatomedin; somatomedin B; somatomedin C; synaptophysin; tumor necrosis factor alpha; animal experiment; animal model; animal tissue; antigen specificity; Article; cell assay; cell function; cell maturation; controlled study; cytokine production; dendritic cell; enzyme phosphorylation; enzyme regulation; female; growth inhibition; human; human cell; immune response; molecular dynamics; mouse; nonhuman; ovary cancer; protein dephosphorylation; protein determination; protein expression; protein function; tumor xenograft; Mus |
顯示於: | 醫學系 |
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