| Objective To investigate the effect of the somatostatin receptor subtype2(SSTR2) on themigration and invasion, the change of epithelial-mesenchymal transition (EMT) of humanpancreatic cancer.Methods Construct3FLAG-puromycin-LV and SSTR2-LV, and transfect hunmanpancreatic cancer cells (Panc-1) respectively. The transfected efficiency was detected byimmunofluorescence. The expression of SSTR2was detected by Real Time PCR andWestern blot. The migration and invasion of Non-transfected cells (blank control group),3FLAG-puromycin-LV transfected cell (negative control group), and SSTR2-LVtransfected cells (experimental group) were assessed by a wound healing assay, a transwellinvasion assay and a transwell migration assay. The changes in morphology of cells wereobserved by optical microscopy. The localization and expression of the epithelial markersand the mesenchymal markers were assayed by immunofluorescence and Western blot.Result The stable mRNA and protein expression of SSTR2was detected in the cellstransfected with SSTR2-LV. The migration and invasion was restrained in the experimentalgroup compared with control groups (P<0.01). Transfection of SSTR2-LV induced amorphologic change of Panc-1cells from fibroblastic shape with cell scattering to a paving stone structure with cell-cell adhesion. In SSTR2-LV-transfected cells, the localization ofE-cadherin was altered from the cytoplasm to cell-cell contacts and the level of Vimentindecreased. Moreover, compare with control groups, the expressions of the epithelialmarkers, E-cadherin and β-catenin, were increased in experimental group; the expressionsof the mesenchymal markers, N-cadherin and Vimentin, were reduced in experimentalgroup.Conclusion Re-expression SSTR2in SSTR2-LV-transfected Panc-1cells induced theincrease expression of epithelial markers and the decrease expression of mesenchymalmarkers, reversed pancreatic cancer EMT, thereby leading to suppress migration andinvasion. |
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