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首页> 外文期刊>Journal of cellular physiology. >JunB can enhance the transcription of IL-8 in oral squamous cell carcinoma
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JunB can enhance the transcription of IL-8 in oral squamous cell carcinoma

机译：JunB可以提高引发口腔的转录鳞状细胞癌

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摘要

Proteasome inhibitor MG132 was shown to enhance the secretion of interleukin 8 (IL-8) by various cells. The enhancement is regulated by the transcription factor activator protein-1 (AP-1) at the transcriptional level. AP-1 is a dimer formed by AP-1 family proteins. The purpose of the present study was to explore the combinations of the AP-1 family proteins that contribute to MG132-driven IL-8 secretion. Oral squamous cell carcinoma-derived cell lines, Ca9-22 and HSC3, were used to demonstrate their response to MG132. IL-8 secretion was augmented by MG132 in both cell lines. c-Jun expression was detected in both the cell lines, whereas c-Fos expression was detected only in the HSC3. The influence of MG132 stimulation on c-Jun and c-Fos expression was further examined by western blot analysis. c-Jun expression was increased by MG132 stimulation, whereas c-Fos expression was not detected even after MG132 stimulation. As JunB is reported to inhibit the transcriptional activity of the AP-1 complex, we speculated that the c-Jun homodimer should contribute to IL-8 enhancement. Expression vectors encoding wild type and c-Jun mutants, M17 and M22-23, respectively, were constructed and transfected into the Ca9-22 cells. In contrast to our expectations, MG132-induced IL-8 secretion was significantly reduced in all the transfectants suggesting that other c-Jun members might form homodimers with c-Jun and contribute to IL-8 enhancement. Transfection of the cells with c-Jun or JunB small hairpin RNA (shRNA) reduced IL-8 secretion up to 50% and 65% of the control shRNA transfectant. Furthermore, cotransfection of both shRNA almost completely inhibited the IL-8 secretion. These results indicate that JunB not only inhibits but also enhances the transcription of c-Jun targets in combination with c-Jun.
机译：蛋白酶体抑制剂MG132增强的分泌白介素8(引发)不同细胞。转录因子激活蛋白1 (AP-1)在转录水平。由AP-1家族蛋白。本研究探讨组合导致AP-1家族的蛋白质MG132-driven引发分泌。carcinoma-derived细胞系,Ca9-22 HSC3,被用来展示他们应对MG132。引发分泌被MG132在增强细胞系。细胞系,而c-Fos表达式只有在HSC3检测到。刺激c-Jun和c-Fos表达通过免疫印迹分析进一步检查。表达增加了MG132刺激,甚至没有发现而c-Fos表达式后MG132刺激。抑制AP-1的转录活动复杂,我们推测c-Jun为应该为引发的提高。向量编码野生型和c-Jun突变体,M17星云和M22-23分别建立了转染到Ca9-22细胞。我们的期望,MG132-induced引发分泌显著降低所有的吗转染子暗示c-Jun其他成员可能会形成为c-Jun和贡献引发增强。JunB c-Jun或者是小发夹RNA(成分)引发分泌减少的50%和65%控制shRNA转染子。cotransfection shRNA几乎完全抑制引发分泌。也表明JunB不仅抑制提高c-Jun目标的转录结合c-Jun。

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