Paclitaxel Induced B7-H1 Expression in Cancer Cells via the MAPK Pathway
Paclitaxel Induced B7-H1 Expression in Cancer Cells via the MAPK Pathway
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DOI：
10.1179/joc.2011.23.5.295
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发表时间：
2011-10-01
影响因子：
1.8
通讯作者：
Yi, Xianjin
中科院分区：
文献类型：
--
作者：
Gong, Wenrong;Song, Qibin;Yi, Xianjin
本研究探讨了化疗药物紫杉醇(PTX)诱导人结肠腺癌细胞系SW480和肝癌细胞系HepG2表达B7-H1免疫抑制分子的机制。免疫荧光和流式细胞仪检测发现PTX诱导SW480和HepG2细胞B7-H1蛋白表达，实时定量聚合酶链式反应(RT-PCR)检测到PTX诱导B7-H1蛋白表达。此外，PTX可诱导两种细胞系ERK1/2的磷酸化。MEK抑制剂U0126可显著阻断PTX诱导的B7-H1mRNA表达上调。而PTX诱导的蛋白表达仅被U0126部分阻断。我们的结果表明，PTX通过转录和转录后机制上调了培养的SW480和HepG2细胞中87-H1的表达。这可能有助于我们更好地理解PTX相关的肿瘤免疫逃避。
In this study, we investigated the mechanisms by which the chemotherapeutic agent paclitaxel (PTX) induced the expression of B7-H1 immunosuppressive molecules in the human colorectal adenocarcinoma cell line SW480 and the hepatocellular carcinoma cell line HepG2. We found PTX induced B7-H1 protein expression in SW480 and HepG2 cells as demonstrated by immunofluorescence and flow cytometry and mRNA expression by using real-time quantitative polymerase chain reaction (PCR). Moreover, PTX treatment induced Erk1/2 phosphorylation in both cell lines. PTX-increased B7-H1 mRNA expression was significantly blocked by MEK inhibitor U0126. However, the protein expression caused by PTX was only partially blocked by U0126. Our results suggest that PTX upregulated 87-H1 expression in cultured SW480 and HepG2 cells via both transcriptional and post-transcriptional mechanisms. This may help us better understand PTX-related tumor immune evasion.