Role of JAK2/STAT3 pathway in EGF-induced invasion and migration of human colon cancer cells

徐建华; 张超; 唐波; 郝迎学; 刘涛; 陈军; 崔浩

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Role of JAK2/STAT3 pathway in EGF-induced invasion and migration of human colon cancer cells

更新时间：2026-01-09

- Role of JAK2/STAT3 pathway in EGF-induced invasion and migration of human colon cancer cells
- Journal of Army Medical University Vol. 32, Issue 7, Pages: 638-641(2010)
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  CLC： R73-37;R730.23;R735.35
- Published：2010
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徐建华,张超,唐波,郝迎学,刘涛,陈军,崔浩.JAK2/STAT3通路在表皮生长因子诱导结肠癌细胞侵袭迁移中的作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(07):638-641.

　Xu Jianhua,Zhang Chao,Tang Bo,Hao Yingxue,Liu Tao,Chen Jun,Cui Hao.Role of JAK2/STAT3 pathway in EGF-induced invasion and migration of human colon cancer cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(07):638-641.
徐建华,张超,唐波,郝迎学,刘涛,陈军,崔浩.JAK2/STAT3通路在表皮生长因子诱导结肠癌细胞侵袭迁移中的作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(07):638-641. DOI：

　Xu Jianhua,Zhang Chao,Tang Bo,Hao Yingxue,Liu Tao,Chen Jun,Cui Hao.Role of JAK2/STAT3 pathway in EGF-induced invasion and migration of human colon cancer cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(07):638-641. DOI：

摘要

目的探讨JAK2/STAT3通路在表皮生长因子（epidermal growth factor

EGF）诱导结肠癌细胞侵袭迁移中的作用。方法以人结肠癌细胞株LoVo 为研究对象

分为对照组、表皮生长因子处理组（EGF组）、表皮生长因子与JAK2 激酶抑制剂AG490共处理组（EGF+AG490组）。采用免疫荧光和Western blot 检测各组LoVo细胞E钙粘素蛋白、磷酸化STAT3表达水平；Transwell法检测细胞侵袭能力；细胞划痕实验检测细胞迁移能力。结果细胞划痕实验对照组细胞划痕闭合约38%，EGF+AG490组细胞划痕闭合约40%，而EGF组闭合约80%。EGF组显著高于另2组（P0.05）；体外侵袭实验显示对照组透膜细胞数为（21.24±2.65）/视野，EGF+AG490组为（23.19±3.50）/视野，EGF组为（55.08±2.14）/视野。EGF组显著高于另2组（P0.05）；与EGF+AG490组结肠癌LoVo细胞相比，EGF组细胞P-STAT3表达增加72.4%，E-cadherin蛋白表达降低68.5%（P0.05）；免疫荧光显示EGF组细胞E-cadherin向细胞质内移位。结论 EGF可通过JAK2/STAT3通路调节E-cadherin在结肠癌LoVo细胞中的表达和定位，增强结肠癌细胞的侵袭迁移能力。

Abstract

Objective To investigate the role of JAK2/STAT3 pathway in the invasion and migration of human colon cancer cells induced by epidermal growth factor (EGF). Methods The human colon cancer cell LoVo were divide into 3 groups

control group

EGF treatment group (10 ng/ml

EGF group)

EGF and AG490 (an inhibitor of JAK2) treatment group (10 ng/ml and 50 μmol/L respectively

EGF+AG490 group). The migration of LoVo cells was measured with scratch assay

and invasion was measured by Transwell chamber. Expressions of P-STAT3 and E-cadherin proteins in the cells were detected by Western blot analysis and immunofluorescence staining. Results Compared with the control and EGF+AG490 group

EGF increased the wound healing [38% vs 40% vs 80%

P0.05]

enhanced the expression of P-STAT3 by 72.4%

and decreased the expression of E-cadherin by 68.5%. The invasion assay demonstrated the number of LoVo cells in EGF group was larger than those of EGF+AG490 and control group (55.08±2.14 vs 23.19±3.50 vs 21.24±2.65

P0.05). In EGF group

E-cadherin was located in the cytoplasm. Conclusion EGF regulates the expression and location of E-cadherin in LoVo cells through JAK2/STAT3 pathway

and increases the migration and invasion of human colon cancer cells.

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