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首页> 外文期刊>The Journal of investigative dermatology. >Modulation of activated leukocyte cell adhesion molecule-mediated invasion triggers an innate immune gene response in melanoma
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Modulation of activated leukocyte cell adhesion molecule-mediated invasion triggers an innate immune gene response in melanoma

机译：激活的白细胞粘附分子介导的入侵的调节触发黑色素瘤的先天免疫基因反应。

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Activated leukocyte cell adhesion molecule (ALCAM/CD166) is a progression marker of a variety of cancers, including melanoma, and is a marker for mesenchymal stem cells. ALCAM expression triggers matrix metalloproteinase activity and correlates with the transition between superficial melanoma growth and deep dermal invasion in vivo. We previously showed that manipulating ALCAM functionality could both decrease and increase melanoma invasion, depending on the manner by which ALCAM function was altered. How ALCAM exerts these opposing invasive phenotypes remained elusive. In the present study, we analyzed differences in melanoma cell gene expression in two-and three-dimensional cultures as function of ALCAM-mediated adhesion. We identified a cluster of genes highly responsive to ALCAM functionality and relevant for melanoma invasion. This cluster is characterized by known invasion-related genes similar to L1 neuronal cell adhesion molecule and showed a remarkable induction of several innate immune genes. Unexpectedly, we identified major variations in the expression of genes related to an immunological response when modulating ALCAM function, including complement factors C1r and C1s. The expression and function of these proteinases were confirmed in protein assays and in vivo. Together, our results demonstrate a link between ALCAM functionality and the immune transcriptome, and support the assumption that ALCAM-ALCAM interactions could function as a cell signaling complex to promote melanoma tumor invasion.
机译：活化的白细胞粘附分子（ALCAM / CD166）是包括黑色素瘤在内的多种癌症的进展标记，并且是间充质干细胞的标记。 ALCAM表达触发基质金属蛋白酶活性，并与浅表黑色素瘤生长和体内深层真皮浸润之间的过渡相关。我们先前表明，根据ALCAM功能的改变方式，操纵ALCAM功能既可以减少也可以增加黑色素瘤的侵袭。 ALCAM如何发挥这些对立的侵袭性表型仍然遥遥无期。在本研究中，我们分析了二维和三维文化中黑色素瘤细胞基因表达的差异，这是ALCAM介导的粘附的功能。我们鉴定了对ALCAM功能高度敏感并与黑色素瘤浸润相关的基因簇。该簇的特征在于与L1神经元细胞粘附分子相似的已知入侵相关基因，并显示出多种先天免疫基因的显着诱导。出乎意料的是，我们在调节ALCAM功能（包括补体因子C1r和C1s）时发现了与免疫反应相关的基因表达的主要变化。这些蛋白酶的表达和功能在蛋白质测定和体内得到证实。在一起，我们的结果证明了ALCAM功能和免疫转录组之间的联系，并支持ALCAM-ALCAM相互作用可以作为促进黑色素瘤肿瘤侵袭的细胞信号复合体起作用的假设。

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