Huang X, Orucevic A, Li M, Gorelik E
University of Pittsburgh Cancer Institute and Department of Pathology, University of Pittsburgh, Pennsylvania 15213, USA.
Clin Exp Metastasis. 2000;18(4):329-35. doi: 10.1023/a:1010867618014.
We have previously found that transfection of BL6-8 melanoma cells with the H-2K, but not H-2D/L genes resulted in loss of their metastatic ability that was associated with decrease in their invasiveness and up-regulation of TIMP-1 expression. In the present study using the methylation-specific PCR (MSP) we found that lack of TIMP-1 expression in BL6-8 is associated with methylation in the TIMP-1 5' regulatory area. In the H-2Kb transfected CL8-1 melanoma cells up-regulation of TIMP-1 was in parallel with loss of TIMP-1 gene methylation. Treatment of BL6-8 with 5-azacytidine or with an inhibitor of histone deacetylase trichostatin A resulted in up-regulation of TIMP-1 expression. These results indicate that methylation and histone deacetylation play an important role in transcription repression of TIMP-1 in BL6 melanoma cells. Some data showed that nitric oxide (NO) could affect methylation and expression of various gene. Therefore we analyzed NO production in B16 melanoma cell lines with different expression of TIMP-1. We have found that B16F10 and BL6-8 melanoma cells do not express TIMP-1 and do not produce nitric oxide (NO) even after stimulation with IFN-gamma and LPS. However, BL6-8 cells transfected with H-2Kb or H-2Kd, but not H-2Dd or H-2Ld gene expressed TIMP-1 and produced NO constitutevely. NO production in these cells was further stimulated by IFN-gamma and LPS. Northern blot analysis showed that expression of iNOS was paralleled with TIMP-1 expression in the tested melanoma cells. However, NO produced by SNAP or inhibition of NO production by NMA did not affect TIMP-1 expression in the tested melanoma cells. Thus, TIMP-1 expression and NO production in BL6 melanoma cells transfected with MHC class I gene coincides but it remains unclear whether NO is responsible for the change in TIMP-1 methylation and expression.
我们之前发现,用H-2K基因而非H-2D/L基因转染BL6-8黑色素瘤细胞会导致其转移能力丧失,这与侵袭性降低及TIMP-1表达上调有关。在本研究中,我们使用甲基化特异性PCR(MSP)发现,BL6-8中TIMP-1表达缺失与TIMP-1 5'调控区的甲基化有关。在H-2Kb转染的CL8-1黑色素瘤细胞中,TIMP-1的上调与TIMP-1基因甲基化的缺失同时发生。用5-氮杂胞苷或组蛋白脱乙酰酶抑制剂曲古抑菌素A处理BL6-8会导致TIMP-1表达上调。这些结果表明,甲基化和组蛋白去乙酰化在BL6黑色素瘤细胞中TIMP-1的转录抑制中起重要作用。一些数据显示,一氧化氮(NO)可影响各种基因的甲基化和表达。因此,我们分析了不同TIMP-1表达的B16黑色素瘤细胞系中的NO产生情况。我们发现,B16F10和BL6-8黑色素瘤细胞即使在受到γ干扰素和脂多糖刺激后也不表达TIMP-1且不产生一氧化氮(NO)。然而,用H-2Kb或H-2Kd而非H-2Dd或H-2Ld基因转染的BL6-8细胞组成性地表达TIMP-1并产生NO。这些细胞中的NO产生进一步受到γ干扰素和脂多糖的刺激。Northern印迹分析表明,诱导型一氧化氮合酶(iNOS)的表达与所测试黑色素瘤细胞中TIMP-1的表达平行。然而,由硝普钠产生的NO或NMA对NO产生的抑制并未影响所测试黑色素瘤细胞中TIMP-1的表达。因此,用I类主要组织相容性复合体(MHC)基因转染的BL6黑色素瘤细胞中TIMP-1的表达和NO的产生是一致的,但尚不清楚NO是否是TIMP-1甲基化和表达变化的原因。