TLR4 signaling induces B7-H1 expression through MAPK pathways in bladder cancer cells
TLR4 signaling induces B7-H1 expression through MAPK pathways in bladder cancer cells
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DOI：
10.1080/07357900801941852
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发表时间：
2008-01-01
影响因子：
2.4
通讯作者：
Zheng, Shusen
中科院分区：
文献类型：
--
作者：
Qian, Yigang;Deng, Junfang;Zheng, Shusen
TLR 4（Toll样受体4）和B7-H1，这是已知的限制在免疫细胞在过去，被发现异常表达在大多数肿瘤细胞，促进肿瘤逃避免疫监视。我们的研究表明，TLR 4信号在膀胱癌细胞中的激活上调B7-H1的表达。此外，ERK或JNK抑制剂可显著减弱这种调节作用。我们的研究结果阐明了TLR 4信号通路调控B7-H1表达的分子机制，并可能为膀胱癌治疗提供下调肿瘤相关B7-H1表达的新策略。
TLR4 (Toll-like receptor 4) and B7-H1, which were known to be restricted to immune cells in the past, were found to be aberrantly expressed in a majority of tumor cells, facilitating tumor evasion from immune surveillance. Our study demonstrated that activation of TLR4 signaling in bladder cancer cells up-regulated B7-H1 expression. Furthermore, this regulation was significantly attenuated by ERK or JNK inhibitor. Our results elucidated the molecule mechanism of regulation of B7-H1 expression through TLR4 signaling and may suggest new strategies of down-regulating the cancer-associated B7-H1 expression for bladder cancer treatment.