2015年12月ONCOLOGY REPORTS杂志（JCR 医学分类下的3 区期刊）发表了赵贵兵题目为“IL-6 mediatesthe signal pathway of JAK-STAT3-VEGF-C promotinggrowth, invasion and lymphangiogenesis in gastric cancer”的研究论文，揭示了IL-6介导JAK-STAT3-VEGF-C信号通路促进胃癌细胞增殖,侵袭及淋巴管生成。

胃癌具有高侵袭和转移的特征，尤其是淋巴结转移，与胃癌患者不良预后密切相关。尽管有证据表明IL-6能促进胃癌的进展，但是具体的机制目前仍知之甚少。我们的研究结果表明,IL- 6及其受体(IL-6 and gp130)广泛表达于各种胃癌细胞系中，包括SGC-7901、MGC803、MKN-28和AGS。IL-6增加了胃癌细胞增殖和侵袭的能力,且可以被JAK抑制剂AG490削弱。此外,外源性IL- 6促进胃癌细胞的VEGF-C表达和人淋巴管内皮细胞的淋巴管生成，JAK抑制剂AG490也能够减弱这些作用。蛋白免疫印迹分析表明,IL-6 能促进胃癌细胞JKA,STAT3 p-STAT3和VEGF-C 蛋白的表达。同时,JKA,STAT3 p-STAT3 and VEGF-C表达能被AG490抑制。因此，我们的实验数据表明IL-6介导JAK-STAT3-VEGF-C信号通路促进胃癌细胞增殖,侵袭及淋巴管生成。此研究表明，IL-6及其相关通路将可能是作为胃癌细胞增殖及淋巴管生成潜在的治疗靶点。

叶建新为本文的通讯作者，朱广伟，黄永健，郑伟，华进，杨树刚，庄金福参与了该课题的研究。该项目得到了福建省科学技术研究重点项目计划，福建省自然科学基金，j9九游会的骨干教师项目，中国非干预胃癌登记调查临床研究项目，卫生部医学科学技术的发展和研究项目，国家临床重点专科建设项目(普通外科) 等基金资助。

Figure 5. AG490inhibits the activity of the IL-6-JAK-STAT3-VEGF-C signal pathway. (A) Westernblot analysis suggested that the IL-6 markedly promoted the expression of JAK,STAT3, p-STAT3 and VEGF-C protein. The promoting effects of IL-6 were abolishedby AG490 treatment in the AGS cells. β-actin protein was used as an internalcontrol. The densitometric value for all groups were normalized to the internalcontrol and relative expression with the protein expression of JAK (B), STAT3(C), p-STAT3 (D) and VEGF-C (E) in AGS group cells were taken as 1. Results areexpressed as mean ± standard deviation (SD), n=3; *P<0.05.