Tan B B, Li Y, Li S J, Zhao Q, Fan L Q, Liu Q W, Zhao Y J, Zhang M Y
The Third Department of Surgery, the Fourth Hospital of Hebei Medical University, Shijiazhuang 050019, China.
Operation Room the Fourth Hospital of Hebei Medical University, Shijiazhuang 050019, China.
Zhonghua Zhong Liu Za Zhi. 2020 Nov 23;42(11):919-924. doi: 10.3760/cma.j.cn112152-20200225-00126.
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.
探讨过氧化物还原酶1（PRDX1）在胃癌细胞上皮间质转化（EMT）中的作用及机制。采用免疫组织化学（IHC）法检测70例胃癌石蜡标本及癌旁正常黏膜中PRDX1蛋白的表达，并分析PRDX1蛋白与临床病理特征的关系。然后合成PRDX1小干扰RNA（siRNA）并转染人胃癌细胞系AGS，采用3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2H四氮唑溴盐（MTT）法检测细胞增殖。采用Transwell小室法检测细胞侵袭能力。利用实时定量聚合酶链反应（RT-qPCR）和蛋白质免疫印迹法检测PRDX1、E-钙黏蛋白、N-钙黏蛋白、波形蛋白和紧密连接蛋白1的表达。胃癌组织中PRDX1蛋白阳性表达率为81.4%，高于正常黏膜组织（27.1%，P<0.05）。PRDX1蛋白表达与胃癌的浸润深度和淋巴结转移有关（P<0.05）。AGS细胞中PRDX1 mRNA和蛋白的表达水平（2.216±0.445，1.212±0.136）高于GES-1细胞（0.342±0.041，0.328±0.038）（P<0.05）。将PRDX1-siRNA转染AGS细胞后，AGS细胞的增殖受到明显抑制（均P<0.05）。转染组AGS细胞的侵袭和迁移率[（112.00±17.98），（50.87±9.79）%]明显低于阴性对照组[（192.50±22.02），（83.03±8.67）%]和空白对照组[（193.83±22.40），（82.40±7.21）%]（均P<0.05）。将PRDX1-siRNA转染AGS细胞后，N-钙黏蛋白、波形蛋白和紧密连接蛋白1的mRNA和蛋白表达降低，而E-钙黏蛋白表达增加（P<0.05）。PRDX1可能通过调节胃癌细胞的EMT促进胃癌的发展。
