TBX2 overexpression promotes proliferation and invasion through epithelial-mesenchymal transition and ERK signaling pathway.

The present study aimed to clarify the clinical significance and biological effects of T-box (TBX)2 and its potential mechanism in gastric cancer (GC). TBX2 protein expression levels in human GC tissues were investigated using immunohistochemistry, and it was demonstrated that TBX2 was overexpressed in 55.9% (90/161) GC samples. TBX2 overexpression correlated with tumor invasion, advanced tumor node metastasis stage and presence of lymph node metastasis. In addition, TBX2 correlated with poor patient survival. To investigate the effect of TBX2 on biological behaviors, TBX2 plasmid transfection was performed in SGC-7901 cells and TBX2 small interfering RNA knockdown was carried out in BGC-823 cells. MTT and matrigel invasion assays demonstrated that TBX2 overexpression promoted proliferation and invasion, whereas TBX2 depletion inhibited proliferation and invasion. TBX2 overexpression also promoted epithelial-mesenchymal transition by downregulating E-cadherin and upregulating N-cadherin. TBX2 overexpression also upregulated matrix metalloproteinase (MMP)2, MMP9, cyclin E and phosphorylated-extracellular signal regulated kinase levels, however downregulated p21. In conclusion, TBX2 may serve as an effective predictor and therapeutic target in human GC.