Elucidation of the mechanism for development and infiltration of cutaneous squamous cell carcinoma

我们证明皮肤鳞状细胞癌（SCC）产生的IL-1α诱导间质成纤维细胞中CD 10的表达。CD 10阳性的成纤维细胞通过金属蛋白酶的诱导降低了支持肿瘤侵袭的P物质的微环境浓度，从而抑制了SCC的侵袭能力。组织蛋白酶K在SCC周围的成纤维细胞中表达，而在良性表皮肿瘤周围的成纤维细胞中不表达。SCC来源的IL-1α诱导CTSK表达上调的成纤维细胞增强了SCC细胞的基质胶侵袭能力，提示基质成纤维细胞在皮肤SCC侵袭中发挥重要作用。

We demonstrated that IL-1αproduction by cutaneous squamous cell carcinoma(SCC) induced CD10 expression in the stromal fibroblast. The CD10-bearing fibroblast inhibited the invasive capacity of SCC by diminishing the microenvironmental concentration of substance P that supports tumor invasion via metalloproteinase induction.Cathepsin K expression was detected in peritumoral fibroblasts around SCC, but not in those surrounding benign epidermal tumors. The CTSK-upregulated fibroblasts generated by SCC-derived IL-1αaugmented the matrigel invasive ability of SCC cells.Taken together, these results highlighted the novel mechanism of stromal fibroblast playing important roles in cutaneous SCC invasion.