Integrin expression in malignant melanoma.
Integrin expression in malignant melanoma.
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整合素在恶性黑色素瘤中的表达。
DOI：
10.1007/bf00046843
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Ramos,DM
中科院分区：
文献类型：
--
作者：
Kramer,RH;Vu,M;Cheng,YF;Ramos,DM
黑色素瘤细胞向间质基质的侵袭是随后局部和远处转移的第一步。侵袭的肿瘤细胞必须在侵袭的早期阶段与细胞外基质相互作用，随后在淋巴和血管的穿透过程中与细胞外基质相互作用。这种与不同类型的细胞外基质的相互作用预示着侵袭细胞必须具有不同配体特异性的表面黏附受体，包括结合不同类型的胶原蛋白和黏附糖蛋白的能力。事实上，转移性黑色素瘤细胞确实表达多种黏附受体，包括整合素异二聚体家族的几种受体。整合素受体既可以对单个配体非常特异，也可以与多个配体结合。肿瘤细胞的黏附受体很可能不仅影响其黏附特性，而且还影响其转移特性。有证据表明，正常黑素细胞具有与黑色素瘤细胞不同的整合素谱。特别是，黑素细胞与层粘连蛋白的粘附性很差，而转移性黑色素瘤细胞与这种配体的粘附性很好。这两种细胞之间的粘附性差异似乎反映了这样一个事实，即黑色素瘤细胞表达黑色素瘤特异性整合素(%MathType！MTEF！2！1！+-%feaafeart1ev1aaatCvAUfeBSjuyZL2yd9gzLbvyNv2CaerbuLwBLn%hiov2DGi1BTfMBaeXafv3ySLgzGmvETj2BSbqefm0B1jxALjhiov2D%aebbfv3ySLgzGueE0jxyaibaiGc9yrFr0xXdbba91rFfpec8Eeeu0x%Xdbba9frFj0-OqFfea0dXdd9vqaq-JfrVkFHe9pgea0dXdar-Jb9hs%0dXdbPYxe9vr0-vr0-vqpWqaaeaabiGaciaacaqabeaadaqaaqGaaO%qaaiaadggadaWgaaWcbaGaamODaaqabaGccqaHYoGydaWgaaWcbaGa%aG4maaqabaaaaa！40cf！)它与层粘连蛋白结合，在正常的黑素细胞中检测不到。黑色素瘤细胞中层粘连蛋白受体的增加和层粘连蛋白结合的增强可能与恶性表型有关。
Invasion of melanoma cells into the underlying interstitial stromal matrix is the initial step for subsequent local and distant metastasis. The invading tumor cell must interact with the extracellular matrix during the early stages of invasion and later during penetration of lymphatic and blood vessels. This interaction with different types of extracellular matrix predicts that the invasive cell must possess surface adhesion receptors with diverse ligand specificities, including the capacity to bind different types of collagens and adhesive glycoproteins. Metastatic melanoma cells do in fact express multiple adhesion receptors, including several of the receptors from the integrin family of heterodimers. The integrin receptors can be either extremely specific for a single ligand or capable of binding multiple ligands. It is likely that the tumor cell's repertoire of adhesion receptors may influence not only its adhesive properties but its metastatic characteristics as well. There is evidence that normal melanocytes have an integrin profile distinct from that of melanoma cells. In particular, melanocytes adhere poorly to laminin while metastatic melanoma cells bind well to this ligand. This difference in adhesion between the two cell types appears to reflect the fact that melanoma cells express a melanoma-specific integrin (% MathType!MTEF!2!1!+-% feaafeart1ev1aaatCvAUfeBSjuyZL2yd9gzLbvyNv2CaerbuLwBLn% hiov2DGi1BTfMBaeXafv3ySLgzGmvETj2BSbqefm0B1jxALjhiov2D% aebbfv3ySLgzGueE0jxyaibaiGc9yrFr0xXdbba91rFfpec8Eeeu0x% Xdbba9frFj0-OqFfea0dXdd9vqaq-JfrVkFHe9pgea0dXdar-Jb9hs% 0dXdbPYxe9vr0-vr0-vqpWqaaeaabiGaciaacaqabeaadaqaaqGaaO% qaaiaadggadaWgaaWcbaGaamODaaqabaGccqaHYoGydaWgaaWcbaGa% aG4maaqabaaaaa!40CF!) that binds laminin and is not detectable in normal melanocytes. The presence of increased laminin receptors and enhanced laminin binding in melanoma cells may contribute to the malignant phenotype.