Study On The Mechanism Of The Effect Of NCAPG On The Proliferation Of Adenocarcinoma Of The Esophagogastric Junction

Objective: Non-SMC condensin I complex subunit G(NCAPG)is a chromosome condensed protein related to mitosis,and one of the non-SMC subunits present in the concentrate I complex.This study explored the effects of NCAPG on the proliferation,invasion,migration and apoptosis of adenocarcinoma of esophagogastric junction(AEG)cell lines,and studied the mechanism of NCAPG in esophagogastric junction adenocarcinoma.And to study the mechanism of NCAPG in esophagogastric junction adenocarcinoma,and explore the possibility of NCAPG in the treatment of adenocarcinoma of esophagogastric junction.Methods: 1.Collect 20 cases of adenocarcinoma of esophagogastric junction,and detect the expression of NCAPG in adenocarcinoma of esophagogastric junction and adjacent tissues by protein profiling technology.2.Analyze the expression level of NCAPG gene in adenocarcinoma of esophagogastric junction tissue in the TCGA database.3.Western Blot and real-time quantitative reverse transcription polymerase chain reaction(q RT-PCR)were used to detect the expression of NCAPG in esophagogastric junction adenocarcinoma cells and normal gastric mucosal cells.4.Construct cell models of NCAPG overexpression and knockdown through plasmids.5.The effects of NCAPG on AEG cells were detected by MTT,clone formation experiment and flow cytometry.6.Exploring the mechanism of NCAPG by immunoblotting.6.Cell proliferation and cell cycle related proteins were observed by Western blotting to explore the mechanism of action of NCAPG 7.After adding PI3K/AKT signaling pathway inhibitor Perofosine to the NCAPG overexpression cell model,will it weaken the effect of NCAPG on esophagogastric junction adenocarcinoma cell lines? 8.The tumorigenic effect of NCAPG was studied in a mouse model,and the results of cell experiments were verified by immunohistochemical methods.Results: 1.Protein profiling showed that NCAPG expression increased in adenocarcinoma of the esophagogastric junction.2.The expression of NCAPG in adenocarcinoma of esophagogastric junction cell lines is increased compared to normal cells.3.Cell experiment shows that NCAPG regulates the G1 phase by up-regulating the cyclins CDK4,CDK6,and cyclin D1 and down-regulating the cell cycle inhibitors P21 and P27 to affect cell proliferation.4.Overexpression of NCAPG increases the levels of phosphorylated PI3 K,AKT and GSK3β proteins.5.In vivo experimental results show that knocking down the expression level of NCAPG can inhibit tumors of adenocarcinoma of esophagogastric junction compared with the control group.Related cyclin CDK4 and proliferation protein Ki-67 protein levels are also suppressed.6.The experimental results show that NCAPG changes cell cycle and proliferation by regulating PI3K/AKT signaling pathway.Conclusion: NCAPG,as an adenocarcinoma gene of the esophagogastric junction,promotes cell proliferation and regulates cell cycle by activating the PI3K/AKT signaling pathway,and plays a very important role in the pathogenesis and progression of adenocarcinoma of esophagogastric junction.Therefore,we believe that NCAPG may be a potential target gene for the treatment of esophagogastric junction adenocarcinoma,and it can regulate the occurrence of esophagogastric junction adenocarcinoma by activating PI3K/AKT signaling.