[Effect and mechanism of PRDX1 in epithelial mesenchymal transformationin of gastric cancer cells].

To explore the effect and mechanism of peroxiredoxin1 (PRDX1) in epithelial mesenchymal transformation (EMT) of gastric cancer cells. The expression of PRDX1 protein was detected by immunohistochemistry (IHC) in 70 paraffin specimens of cancer and normal mucosa adjacent to gastric cancer, and the relationship between PRDX1 protein and clinicopathological characteristics was analyzed. Then PRDX1-small interfering RNA (siRNA) was synthetized and transfected into human gastric cancer cell line AGS, and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) assay was used to test cell proliferation. Transwell chamber assay was employed to test invasion of cells. Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were utilized to test the expressions of PRDX1, E-cadherin, N-cadherin, vimentin, and claudin-1. The positive rate of PRDX1 protein expression in gastric cancer was 81.4%, higher than that in normal mucosa (27.1%, <0.05). The expression of PRDX1 protein was related to invasive depth and lymph node metastasis of gastric cancer (<0.05). The expressions of PRDX1 mRNA and protein in AGS cells (2.216±0.445, 1.212±0.136), were higher than those in GES-1 cells (0.342±0.041, 0.328±0.038) (<0.05). When PRDX1-siRNA was transfected into AGS cells, the proliferation of AGS cells was significantly inhibited (all <0.05). The invasion and migration rate of AGS cells in the transfection group [(112.00±17.98), (50.87±9.79)%] were significantly lower than those of the negative control group [(192.50±22.02), (83.03±8.67)%] and blank control group [(193.83±22.40), (82.40±7.21)%] (all <0.05). The expressions of mRNA and protein of N-cadherin, vimentin and claudin-1 decreased, while the expression of E-cadherin increased when PRDX1-siRNA was transfected into AGS cells (<0.05). PRDX1 may promote the development of gastric cancer by regulating the EMT of gastric cancer cells.