Expression of STAT3, MMP-1 and TIMP-1 in gastric cancer and correlation with pathological features

The aim of this study was to investigate the mRNA and protein expression of STAT3, MMP-1 and TIMP-1 in gastric cancer (GC), and to explore the correlations between these proteins and the biological behaviors of GC. Reverse transcription-polymerase chain reaction was employed to detect the mRNA expression of STAT3, MMP-1 and TIMP-1 in GC tissues (n=30), adjacent normal tissues (n=30) and superficial gastritis (SG) tissues (n=30). Immunohistochemistry was performed using the SP method to measure the protein expression of STAT3 (unphosphorylated), MMP-1 and TIMP-1. The correlation between the pathological features of GC and STAT3, MMP-1 as well as TIMP-1, were evaluated. The mRNA expression of STAT3 in GC tissues (0.821±0.128) was significantly higher compared to that in adjacent normal tissues (0.355±0.100) and SG tissues (0.398±0.096) (P<0.05). The mRNA expression of MMP-1 in GC tissues (0.749±0.133) was significantly increased compared to adjacent normal tissues (0.335±0.106) and SG tissues (0.345±0.063) (P<0.05). The mRNA expression of TIMP-1 in GC tissues (0.386±0.125) was comparable to that in adjacent normal tissues (0.343±0.078) and SG tissues (0.345±0.061), but the mRNA expression of TIMP-1 in GC tissues was significantly correlated with the differentiation of GC cells and lymph node metastasis. STAT3, MMP-1 and TIMP-1 were significantly associated with the differentiation of GC cells and lymph node metastasis, but not related to age, gender and tumor size. The positive rate of unphosphorylated STAT3 expression was dramatically higher in GC tissues (86.7%) compared to that in adjacent normal tissues (16.7%) and SG tissues (10.0%) (P<0.05). The positive rate of MMP-1 protein expression in GC tissues (63.3%) was significantly higher compared to that in adjacent normal tissues (13.3%) and SG tissues (16.7%) (P<0.05). However, no significant difference was observed in the TIMP-1-positive rate among the three groups (23.3, 16.7 and 10.0%, respectively; P>0.05). STAT3 and MMP-1 may be involved in the development and metastasis of GC, and treatment targeting TIMP-1 may be a promising strategy.