Study On The HDAC4/miR-200a Feedback Loop Regulates Proliferation,Invasion And Metastasis Of Gastric Cells

Objective: To clarify the expression of HDAC4 and mi R-200 a in gastric cancer tissues,to explore the effects of HDAC4/mi R-200 a feedback loops on the proliferation,invasion,and metastasis of gastric cancer cells.Provide more evidence for the treatment of gastric cancer,and find potential new targets for the treatment of gastric cancer.Methods: The specimens of cancer tissues and adjacent tissues from 40 patients with gastric cancer were selected,and the expression of HDAC4 was detected by immunohistochemistry.At the same time,the expression of HDAC4 m RNA and mi R-200 a in the above 40 samples were detected by fluorescent quantitative PCR.In BGC-823 gastric cancer cell lines,plasmids were used to up-regulate HDAC4 expression,si RNA was down-regulation of HDAC4 expression,and mi R-200 a expression was detected by fluorescent quantitative PCR;Lentiviral transfection was used to up-regulate mi R-200 a expression and HDAC4 expression was detected by western-bolt.Western-bolt detection was used to detect the above-mentioned transfected cells ZEB1,ZEB2,epithelial cell markers E-cadherin and interstitial cell markers N-cadherin and vimentin(Vimentin).Ed U cell proliferation detection kit and Cell Counting Kit-8 reagent were used to detect the cell proliferation ability,and transwell cells were used to detect the gastric cancer cell invasion and metastasis ability.All experimental data results are expressed as mean±standard deviation(mean±SD).All data were analyzed using spss 24.0 software.The expression of RNA in gastric cancer tissues and adjacent tissues was tested by Wilcoxon rank sum test.The correlation between the two Pearson correlation coefficients were used,and the remaining data were analyzed by t test,with P≤0.05 as statistically significant.Result: 1.Compared with adjacent cancer tissues,the expression of HDAC4 m RNA is up-regulated in gastric cancer tissues,while the expression of mi R-200 a is down-regulated in gastric cancer tissues.There was a negative correlation between HDAC4 m RNA and mi R-200 a expression.2.Down-regulating the expression of HDAC4 will increase the expression of mi R-200 a,and up-regulating the expression of HDAC4 will decrease the expression of mi R-200 a.3.Up-regulating the expression of mi R-200 a will inhibit the expression of HDAC4.4.HDAC4 promotes epithelial-mesenchymal transition in gastric cancer cells,mi R-200 a inhibits epithelial-mesenchymal transition in gastric cancer cells 5.HDAC4 promotes the proliferation,invasion and metastasis of gastric cancer cells,and mi R-200 a inhibits the proliferation,invasion and metastasis of gastric cancer cells.Conclusion: 1.HDAC4 can regulate the expression of mi R-200 a in gastric cancer cells,and at the same time mi R-200 a can also regulate the expression of HDAC4,which indicates that there is a mutually-regulated feedback regulation loop between HDAC4 and mi R-200 a.2.HDAC4/mi R-200 a feedback regulation circuit promotes epithelial-mesenchymal transition(EMT)of gastric cancer cells.3.HDAC4/mi R-200 a feedback regulation circuit promotes the proliferation,invasion and metastasis of gastric cancer cells.