Study On Allicin Induces The Molecule Of Middle Retarding Effect In Gastric Cancer Cells Mechanism

Objective In this study,i TRAQ proteomics technology and IPA bioinformatics analysis platform were used to screen differentially expressed proteins in DATS induced gastric cancer cells,and to investigate the molecular mechanism of DATS induced mitotic crisis.Methods 1.The effects of allicin(0μmol/L,25μmol/L,50μmol/L,100μmol/L)on cell cycle and mitotic crisis of gastric cancer BGC823 cells were determined by flow cytometry,so as to select the optimal drug concentration and action time.2.ITRAQ proteomics was used to screen out differentially expressed proteins in synchronous and non-synchronous groups of gastric cancer BGC823 cells.3.IPA was used to analyze the diseases,functions and regulatory effects of these differentially expressed proteins.Results 1.Allicin can arrest the cell cycle of gastric cancer BGC823 cells in G2/M phase and induce mitotic crisis,and the inhibitory effect on BGC823 cells was most obvious when allicin concentration was 25 μmol/L and treatment time was 12 h.2.ITRAQ quantitative proteomics results showed that allicin in the non-synchronous group could induce the differential expression of 458 proteins in gastric cancer BGC823 cells,of which 85 proteins were up-regulated and 373 proteins were down-regulated.In the synchronous group,allicin could induce the differential expression of 127 proteins in gastric cancer BGC823 cells,of which 81 proteins were up-regulated and 46 proteins were down-regulated.3.IPA analysis showed that the differentially expressed proteins were mainly concentrated in diseases and functions such as cancer,cell death and survival,body injury and abnormality,tumor morphology,and RNA post-transcriptional modification;The most significant regulatory effect is that FOS and other regulators can inhibit endothelial cell adhesion and tumor cell migration through ALCAM and other genes.Conclusion 1.Allicin(25μmol/L,12 h)inhibited the proliferation of gastric cancer BGC823 cells,and significantly blocked the cell cycle in G2/M phase and induced mitotic crisis.2.The molecular mechanism of mid-stage block in gastric cancer BGC823 cells under allicin intervention may be related to ARRDC3,RP family,Haus3,SETDB1 and other differentially expressed proteins.These differential proteins were involved in biological processes and diseases that may involve the ubiquitin proteasome pathway in eukaryotic cells,biosynthesis of ribosomal proteins,tumor cell death,organ damage and abnormalities,and RNA post-transcriptional modification.These results suggested that these processes may be related to allicin induced mid-phase arrest of gastric cancer cells.3.Allicin may inhibit endothelial cell adhesion and tumor cell migration through the expression of FOS,ALCAM and other differential proteins.