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