首页> 美国卫生研究院文献>British Journal of Cancer >Downregulation of miR-302c and miR-520c by 125(OH)2D3 treatment enhances the susceptibility of tumour cells to natural killer cell-mediated cytotoxicity
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Downregulation of miR-302c and miR-520c by 125(OH)2D3 treatment enhances the susceptibility of tumour cells to natural killer cell-mediated cytotoxicity

机译:125(OH)2D3处理下调miR-302c和miR-520c增强了肿瘤细胞对自然杀伤细胞介导的细胞毒性的敏感性

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摘要

Background: NKG2D recognises several ligands, including polymorphic major histocompatibility complex class I chain-related chain-related proteins A and B (MICA/B) and unique long 16-binding proteins (ULBPs). These ligands are present on cancer cells and are recognised by NKG2D in a cell-structure-sensing manner, triggering natural killer (NK) cell cytotoxicity. However, the mechanisms that control the expression of NKG2D ligands in malignant cells are poorly understood. 1-α,25-Dihydroxyvitamin D3 (1,25(OH)2D3) was recently shown to enhance the susceptibility of melanoma cells to the cytotoxicity of NK cells. However, the function of 1,25(OH)2D3 in other cancers and its potential mechanisms of action remain unknown.
机译:背景:NKG2D识别几种配体,包括多态性主要组织相容性复合物I类链相关链相关蛋白A和B(MICA / B)和独特的长16结合蛋白(ULBPs)。这些配体存在于癌细胞上,并被NKG2D以细胞结构感知的方式识别,从而触发自然杀伤(NK)细胞的细胞毒性。然而,人们对控制NKG2D配体在恶性细胞中表达的机制了解甚少。最近显示1-α,25-二羟基维生素D3(1,25(OH)2D3)增强了黑素瘤细胞对NK细胞的细胞毒性的敏感性。但是,1,25(OH)2D3在其他癌症中的功能及其潜在的作用机制仍然未知。

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