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紫杉醇通过丝裂原活化蛋白激酶(MAPK)信号通路诱导癌细胞中B7-H1的表达。

Paclitaxel induced B7-H1 expression in cancer cells via the MAPK pathway.

作者信息

Gong Wenrong, Song Qibin, Lu Xiaoming, Gong Wensheng, Zhao Jianhua, Min Peng, Yi Xianjin

机构信息

Department of Clinical Laboratory, the Affiliated Hospital of XiangFan University, XiangFan 441021, Hubei, China.

出版信息

J Chemother. 2011 Oct;23(5):295-9. doi: 10.1179/joc.2011.23.5.295.

Abstract

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 Erk½ 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 B7-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.

摘要

在本研究中,我们探究了化疗药物紫杉醇(PTX)诱导人结肠腺癌细胞系SW480和肝癌细胞系HepG2中B7-H1免疫抑制分子表达的机制。我们发现,通过免疫荧光和流式细胞术证实,PTX可诱导SW480和HepG2细胞中B7-H1蛋白表达,利用实时定量聚合酶链反应(PCR)检测其mRNA表达。此外,PTX处理可诱导这两种细胞系中的Erk½磷酸化。MEK抑制剂U0126可显著阻断PTX诱导的B7-H1 mRNA表达增加。然而,U0126仅部分阻断了PTX引起的蛋白表达。我们的结果表明,PTX通过转录和转录后机制上调培养的SW480和HepG2细胞中B7-H1的表达。这可能有助于我们更好地理解与PTX相关的肿瘤免疫逃逸。

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