c-myb 激活 T47D 和 MCF7 乳腺癌细胞中的 CXCL12 转录。
c-myb activates CXCL12 transcription in T47D and MCF7 breast cancer cells.
机构信息
Department of Breast Surgery, Breast Cancer Institute, Cancer Hospital/Cancer Institute, Fudan University, Shanghai, China.
出版信息
Acta Biochim Biophys Sin (Shanghai). 2010 Jan;42(1):1-7. doi: 10.1093/abbs/gmp108.
Chemokine C-X-C motif ligand 12 (CXCL12) is a potent chemotactic and angiogenic factor that has been proposed to play a role in organ-specific metastasis and angiogenic activity in several malignancies. In this study, we found that the overexpression of c-myb could elevate CXCL12 mRNA level and CXCL12 promoter activity in human T47D and MCF-7 breast cancer cells. Chromatin immunoprecipitation assay demonstrated that c-myb could bind to the CXCL12 promoter in the cells transfected with cmyb expression vector. c-myb siRNA attenuated CXCL12 promoter activity and the binding of c-myb to the CXCL12 promoter in T47D and MCF-7 cells. These results indicated that c-myb could activate CXCL12 promoter transcription.
趋化因子 C-X-C 基元配体 12（CXCL12）是一种有效的趋化因子和血管生成因子，据推测其在几种恶性肿瘤的器官特异性转移和血管生成活性中发挥作用。在这项研究中，我们发现 c-myb 的过表达可以提高人 T47D 和 MCF-7 乳腺癌细胞中 CXCL12 mRNA 水平和 CXCL12 启动子活性。染色质免疫沉淀测定表明，c-myb 可以与转染 cmyb 表达载体的细胞中的 CXCL12 启动子结合。c-myb siRNA 减弱了 T47D 和 MCF-7 细胞中 CXCL12 启动子活性和 c-myb 与 CXCL12 启动子的结合。这些结果表明 c-myb 可以激活 CXCL12 启动子转录。
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