Gong Wenrong, Song Qibin, Lu Xiaoming, Gong Wensheng, Zhao Jianhua, Min Peng, Yi Xianjin
Department of Clinical Laboratory, the Affiliated Hospital of XiangFan University, XiangFan 441021, Hubei, China.
J Chemother. 2011 Oct;23(5):295-9. doi: 10.1179/joc.2011.23.5.295.
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.
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。
