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细胞黏附与通讯蛋白在黑色素瘤进展模型中呈现差异性表达。

Cell adhesion and communication proteins are differentially expressed in melanoma progression model.

机构信息

Department of Skin Oncology, Hospital AC Camargo, São Paulo, SP, Brazil.

出版信息

Hum Pathol. 2011 Mar;42(3):409-18. doi: 10.1016/j.humpath.2010.09.004. Epub 2010 Dec 28.

Abstract

Cutaneous melanoma is an aggressive cancer derived from skin melanocytes. Tissue microarrays are being used to evaluate the roles of numerous proteins implicated in some of the pathways involved in melanoma pathogenesis. Based on a previous study using a complementary DNA microarray platform, the aim of this study was to evaluate the immunohistochemical expression of the adhesion and communication molecules connexin 43, desmocollin 3, cytokeratin 5, kallikrein 6, and kallikrein 7 in a melanoma progression model. We analyzed 59 common nevi, 22 atypical nevi, and 162 invasive and 29 metastatic melanomas on tissue microarrays using digital microscopy. The expression of desmocollin 3 and connexin 43 was higher in melanomas (P < .001). Kallikrein 6 expression was higher in melanomas than in common nevi (P < .006). The expression of cytokeratin 5 and kallikrein 7 was higher in atypical nevi than in melanomas (P < .001) and was higher in melanomas than in common nevi (P < .001). The expression of desmocollin 3 and connexin 43 in melanomas indicates loss of cell-cell interactions, which starts in the early steps of the melanoma progression model. Keratin expression in melanomas may play a particular role during melanocyte development. The expression of kallikrein 7 and kallikrein 6 in melanomas may be responsible for the loss of cell-cell adhesion.

摘要

皮肤黑色素瘤是一种源自皮肤黑素细胞的侵袭性癌症。组织微阵列正在被用于评估许多在黑色素瘤发病机制相关途径中起作用的蛋白质的作用。基于之前使用 cDNA 微阵列平台的研究,本研究旨在评估细胞黏附与通讯分子连接蛋白 43、桥粒芯胶蛋白 3、细胞角蛋白 5、激肽释放酶 6 和激肽释放酶 7 在黑色素瘤进展模型中的免疫组织化学表达。我们在组织微阵列上使用数字显微镜分析了 59 个普通痣、22 个不典型痣、162 个侵袭性和 29 个转移性黑色素瘤。桥粒芯胶蛋白 3 和连接蛋白 43 在黑色素瘤中的表达更高(P<.001)。激肽释放酶 6 在黑色素瘤中的表达高于普通痣(P<.006)。细胞角蛋白 5 和激肽释放酶 7 在不典型痣中的表达高于黑色素瘤(P<.001),在黑色素瘤中的表达高于普通痣(P<.001)。黑色素瘤中桥粒芯胶蛋白 3 和连接蛋白 43 的表达表明细胞-细胞相互作用的丧失,这始于黑色素瘤进展模型的早期阶段。黑色素瘤中的角蛋白表达可能在黑素细胞发育过程中发挥特殊作用。激肽释放酶 7 和激肽释放酶 6 在黑色素瘤中的表达可能导致细胞-细胞黏附的丧失。

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