SOCS3对结肠癌增殖和侵袭的调控机制

目的探讨细胞因子信号抑制子3（SOCS3）对结肠癌增殖与侵袭能力的调控机制。方法收集我院2014年7月~2017年5月进行肿瘤治疗并经确诊的80例结肠癌患者的癌组织（n=80）和癌旁组织标本（n=80）。通过Western blot分析SOCS3在组织中表达情况。复苏结肠癌细胞系SW480，利用lipo3000转染建SOCS3的过表达质粒；利用小干扰RNA（siRNA）技术转染结肠癌细胞株敲低SOCS3表达。应用CCK-8检测SOCS3基因对结肠癌细胞增殖的影响；采用Transwell试验测定SOCS3基因对于SW480侵袭能力的作用。通过去甲基化及IL-6处理SW480观察对于SOCS3表达的影响，并检测处理之后对SW480增殖、侵袭的作用。结果结肠癌组织中SOCS3表达量均低于癌旁组织；过表达SOCS3后抑制SW480细胞增殖和侵袭，而敲减SOCS3后促进其增殖和侵袭；去甲基化处理SW480上调了SOCS3的表达，SW480增殖和侵袭能力受到抑制；IL-6处理SW480后降低了SOCS3的表达，SW480细胞增殖和侵袭能力得以增强。结论SOCS3参与结肠癌的发生发展，是结肠癌治疗的潜在靶点。在结肠癌患者中，SOCS3低表达可能与甲基化有关。

Role of cytokine signal suppressor 3 in the regulatory mechanism of colon cancerinvasion and proliferation

Objective To investigate the expression of cytokine signal suppressor 3 (SOCS3) in colon cancer tissue and themechanism by which SOCS3 regulates the proliferation and invasion of colon cancer. Methods We collected the specimens oftumor tissues and paired adjacent tissues from 80 patients with colon cancer undergoing radical resection in our hospitalbetween July, 2014 and May, 2017, and the expression of SOCS3 in the tissue samples was analyzed using Western blotting. Wealso transfected colon cancer cell line SW480 with a SOCS3-overexpressing plasmid or a small interference RNA (siRNA) forSOCS3 knockdown, and the changes in the cell proliferation and invasion capacity were evaluated using CCK-8 assay andTranswell assay, respectively. The effect of demethylation and IL-6 treatment on SOCS3 expression and the proliferation andinvasion of SW480 cells were observed. Results Colon cancer tissues showed a lowered expression of SOCS3 compared withthe adjacent tissues. Over-expression of SOCS3 significantly inhibited while SOCS3 knockdown obviously promoted theproliferation and invasion of SW480 cells in vitro. Demethylation treatment up-regulated SOCS3 expression and inhibited theproliferation and invasion capacity of SW480 cells; IL-6 treatment of the cells caused the reverse changes. Conclusion SOCS3participates in the development and progression of colon cancer and serves as a potential target for colon cancer treatment. Inpatients with colon cancer, the low expression of SOCS3 possibly as a result of methylation may promote the proliferation andinvasion of the cancer cells.