Objectives: Trefoil factor family is expressed in several tissues of the body and provides gastric and intestinal protection and healing. This research aims to indicate the mechanism involved in its function.

Methods: The intestinal epithelial cells were pretreated with JAK inhibitor AG490 or the concentration of 60ug/ml human recombinant trefoil factor, while the levels of phospho-STAT3, E-cadherin and N-cadherin were detected by Western Blotting. The levels of Matrix Metalloproteinases, Ecadherin and N-cadherin were evaluated by quantitative real time PCR. The cell migration was assessed by the transwell assay and the scratch assay. The immunofluorescence method was performed to detect the reduction of molecular E-cadherin.

Results: hTFF3 activates the JAK/STAT3 pathway in HT-29 cells. The effect of JAK/STAT3 pathway mechanism on cell migration promoted by hTFF3. TFF3 promoting cell migration is associated with increased gene transcription of MMPs. hTFF3 alters E-cadherin expression. hTFF3 activates the expression of N-cadherin and down-regulates E-cadherin expression in HT-29 Cells.

Conclusion: We have shown that TFF3 activated the JAK/STAT3 pathway. TFF3 increased the level of Matrix Metalloproteinases and N-cadherin, decreased that of E-cadherin, while AG490 had the opposite effect. TFF3 accelerated cell migration and the AG490 relieved the migrating rate to control the levels. TFF3 activated JAK/STAT3 pathway which was associated with intestinal epithelial cell migration.

目标：三叶因子家族在人体的多个组织中表达，并提供胃和肠的保护和愈合。这项研究旨在指出参与其功能的机制。

方法：用JAK抑制剂AG490或60ug / ml人重组三叶因子预处理肠道上皮细胞，Western Blotting检测其磷酸化STAT3，E-cadherin和N-cadherin的水平。通过定量实时PCR评估基质金属蛋白酶，钙黏着蛋白和N钙黏着蛋白的水平。通过transwell测定法和刮擦测定法评估细胞迁移。进行了免疫荧光法以检测分子E-钙粘蛋白的还原。

结果：hTFF3激活HT-29细胞中的JAK / STAT3途径。JAK / STAT3途径机制对hTFF3促进的细胞迁移的影响。TFF3促进细胞迁移与MMPs基因转录增加有关。hTFF3改变E-钙粘蛋白的表达。hTFF3激活HT-29细胞中N-钙粘蛋白的表达并下调E-钙粘蛋白的表达。

结论：我们已经证明TFF3激活了JAK / STAT3途径。TFF3增加了基质金属蛋白酶和N-钙粘蛋白的水平，降低了E-钙粘蛋白的水平，而AG490具有相反的作用。TFF3加速了细胞迁移，而AG490降低了迁移速率以控制水平。TFF3激活了与肠上皮细胞迁移相关的JAK / STAT3途径。