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目的检测大肠癌(CRC)中IL-6、SOCS3基因mRNA表达和启动子甲基化状态,以及STAT3基因mRNA表达水平,探讨大肠癌中IL-6、SOCS3基因表观遗传学改变及其对IL-6/STAT3通路的影响。方法实时荧光定量PCR检测20例CRC癌组织及癌旁组织IL-6、SOCS3及STAT3基因mRNA水平,甲基化特异性PCR(MSP)检测SOCS3甲基化状态,亚硫酸氢盐测序(BSP)检测IL-6启动子甲基化状态。结果与癌旁组织相比,癌组织中IL-6、STAT3 mRNA表达显著增高(P<0.05),而SOCS3显著降低,IL-6与SOCS3表达呈负相关;癌组织中IL-6启动子-633、-611、-575、-575bp位点甲基化水平均降低,而SOCS3则呈现高度甲基化状态(P<0.05)。结论大肠癌中IL-6和SOCS3基因DNA甲基化状态异常,影响基因表达,从而诱导IL-6/STAT3信号转导通路持续活化,促进了大肠癌的发生发展。
Objective To detect the mRNA expression of IL-6, SOCS3 and methylation status of STAT3 in colorectal cancer (CRC) and the expression of STAT3 mRNA in colorectal cancer, and to explore the changes of IL-6 and SOCS3 gene in colorectal carcinoma -6 / STAT3 pathway. Methods The mRNA levels of IL-6, SOCS3 and STAT3 were detected by real-time fluorescence quantitative PCR in 20 cases of CRC and paracancerous tissues. The methylation-specific PCR (MSP) was used to detect the status of SOCS3 methylation and bisulfite sequencing (BSP) The methylation status of IL-6 promoter was detected. Results Compared with adjacent normal tissues, the expression of IL-6 and STAT3 mRNA in cancer tissue was significantly increased (P <0.05), but SOCS3 was significantly decreased, while the expression of IL-6 and SOCS3 was negatively correlated. The expression of IL-6 promoter- The methylation levels of 633, -611, -575 and -575bp sites were decreased, while SOCS3 was highly methylated (P <0.05). Conclusion The abnormal DNA methylation status of IL-6 and SOCS3 gene in colorectal cancer affects the gene expression, which leads to the sustained activation of IL-6 / STAT3 signal transduction pathway and the promotion of the development of colorectal cancer.