ABSTRACT
Objective The aim of this study was to investigate the relative expression of zinc finger protein ZNF436 in hu-man gastric cancer cells and tissues and its mechanism of ZNF436 on migration and invasion of gastric cancer MKN -28 cells. Methods RT-qPCR and immunohistochemistry were used to determine the expression of ZNF436 at the levels of mRNA and pro-tein in human gastric cancer cells,gastric cancer and matched paracancerous tissues,and normal human gastric tissues. ZNF436 ex-pression and prognostics were analyzed through online data. The ZNF436 -siRNA ( experimental group) and NC -siRNA( control group)plasmids were transfected into MKN028 cells. RT-qPCR was used to confirm the knockout efficiency of ZNF436 after trans-fection for 48 hours. The transwell assay was used to analyze the effect of ZNF436 on cell migration and invasion after knockout ZNF436. The effect of ZNF436 on cell metastasis was verified by nude mice metastasis experiments. The effect of ZNF436 on WNT/β-catenin signaling pathway was verified by immunoblotting. Results Compared with normal gastric epithelial cells,ZNF436 was highly expressed in human gastric cancer cells(P<0. 001). ZNF436 was highly expressed in gastric cancer tissues compared with ad-jacent normal tissues and normal human gastric tissues(P<0. 001). The expression of ZNF436 was associated with the prognosis of gastric cancer from online data(P=0. 0028);the high expression of ZNF436 gene,the worse prognosis of patients(P<0. 001);When compared with the control group,the migration and invasion ability in the experimental group was significantly inhibited(P<0. 001);the size and volume of metastasis in nude mice in the experimental group were significantly lower than those in the experimental group ( P<0. 001). After the low expression of ZNF436,the WNT/β-catenin signaling pathway and its downstream cytokines were signifi-cantly inhibited. Conclusion ZNF436 is up-regulated as a potential oncogene in human gastric cancer and participates in the pro-gression of gastric cancer by promoting WNT/β-catenin signaling pathway.