Cyclosporin A upmodulates the alpha-subunit of the interleukin-2 receptor and the metastatic ability of murine B16F10 melanoma cells.

M D Boyano, A G de Galdeano, M D García-Vázquez, A Alvarez, M Luz Cañavate
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引用次数: 4

Abstract

In the present study, the effect of in vitro cyclosporin A (CsA) treatment on IL-2R expression and the metastatic behavior of B16F10 melanoma cells has been reported. CsA treatment was found to increase the percentage of B16F10 cells expressing the alpha-subunit of IL-2R on the cell surface and also at the mRNA level. Moreover, CsA treated B16F10 cells also express the beta-subunit of IL-2. In vivo experiments showed that CsA increases the affinity of B16F10 metastazing cells for the liver and decreases that for the lung. CsA modulated the expression of MHC class I and class II antigens, but no significant differences in the resistance of CsA-treated B16F10 cells to NK lysis were observed. Finally, proliferation of B16F10 cells in the presence of several doses of CsA did not vary and CsA increased the amount of IL-1beta mRNA expression. These results suggest that CsA, through the modulation of cytokines and MHC antigen expression on B16F10 cells, could have an effect upon the metastatic progression of the B16F10 melanoma.

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环孢素A上调白细胞介素-2受体α亚基和小鼠B16F10黑色素瘤细胞的转移能力。
本研究报道体外环孢素A (cyclosporin A, CsA)治疗对B16F10黑色素瘤细胞IL-2R表达及转移行为的影响。发现CsA处理增加了B16F10细胞在细胞表面和mRNA水平上表达IL-2R α亚基的百分比。此外,CsA处理的B16F10细胞也表达IL-2的β亚基。体内实验表明,CsA增加了B16F10转移细胞对肝脏的亲和力,降低了对肺的亲和力。CsA可调节MHC I类和II类抗原的表达,但CsA处理的B16F10细胞对NK裂解的抗性无显著差异。最后,在不同剂量CsA存在下,B16F10细胞的增殖没有变化,CsA增加了il -1 β mRNA的表达量。这些结果表明,CsA可能通过调节B16F10细胞的细胞因子和MHC抗原表达,影响B16F10黑色素瘤的转移进展。
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