Objective To study the influence of O-GlcNAcylation on on proliferation and invasion of gastric cancer cells and evaluate the role of Aktl on O-GlcNAcylation promotting cells proliferation and invasion in gastric cancer.Methods Build the cell model:O-GlcNAc glycosylation levels rise or fall.The cell viability was determine by MTT.To investigate whether O-GlcNAcylation affected colony formation ability of gastric cancer cells,soft agar colony assays were carried out.Cell migration or invasion was using transwell chambers.The expression of Akt1 was detected through Western blot.Thiamet-G was used to eualuate the role of Akt1 on O-Gcnac cylation regulating invasion in gastric Cancei.Results O-GlcNAcylation was increased the gastric cancer cells proliferation ability,colony formation ability,migration and invasion ability in vitro.Akt1 was activated by Ser473 phosphorylation upregulation though O-GlcNAcylation.Akt1 shRNA was inhibition the cell invasive which induced by Thiamet-G.Akt1 overexpression was promoted by Thiamet-G-induced cell invasion.Conclusion O-GlcNAcylation enhanced oncogenic phenotypes possibly partially involving Akt1.

Objective To investigate the influence of GTPBP4 gene expression down-regulation in hepatocellular carcinoma (HCC) cell line SMMC-7721 on the intracellular and extracellular biological behaviors and its action mechanism.Methods The differences of GTPBP4 expression level in HCC tissues and paracancerous tissues were compared by using the immunohistochemical method.The expression of GTPBP4 mRNA in 4 kinds of HCC cell line(SMMC-7721,HEPG2,HUH-7,HEP3B) was detected by using the real-time fluorescent quantitative PCR(RT-PCR).The expression of GTPBP4 in HCC cell line SMMC-7721 was downregulated by using the RNA interference technique and the cellular biological behavior change was observed.Results In HCC histological chip,the expression level of GTPBP4 protein in HCC tissue was significantly higher than that in para-cancerous tissue.GT-PBP4 was also significantly up-regulated in 4 kinds of HCC cell line.After the expression of GTPBP4 was down-regulated,the proliferation ability of HCC cells was weakened and apoptosis was increased.The cells in S phase and G1.phase had no significant changes,but which in G2 phase were increased,the ability of in vitro clone formation was weakened,the nude mouse in vivo tumor formation capacity was weakened.The expressional profiles microarray results showed that 333 genes were changed in SMMC-7721 cells after GTPBP4 knockdown,in which the up-regulated genes were 134,the down-regulated genes were 199.The channel enrichment analysis found 10 signal transduction pathways of the enriched differential genes.Western blot showed that the expression levels of CCND1,CCND2,CDK6 and MDM2 were changed significantly after GTPBP4 expression down-regulation.Conclusion GT-PBP4 as a promoting HCC gene may influence HCC biological behavior possibly by regulating the expression of key gene in cell cycle.

Objective : To explore the regulatory mechanism of the long noncoding FGD5⁃AS1 ( LncRNA FGD5⁃AS1) on hepatocellular carcinoma(HCC)progression. Methods : The expression level of FGD5 ⁃AS1 was measured in tumor tissues and cell lines by RT⁃qPCR. CCK⁃8 , EdU , flow cytometry , wound healing and transwell chamber assays were performed to investigate the role of FGD5 ⁃AS1 in HCC cell proliferation , apoptosis , migration and invasion in vitro. At the molecular level , dual luciferase reporter and RNA pull down assays were performed to identify the interaction among FGD5 ⁃AS1 , miR⁃873 ⁃5p and GTPBP4. Results : FGD5 ⁃AS1 was upregulated in HCC tissues and cells. Moreover, FGD5 ⁃AS1 knockdown suppressed HCC cell proliferation , migration and invasion , and induced apoptosis in vitro. Mechanistically , FGD5 ⁃AS1 directly bound to miR⁃873 ⁃5p and competitively inhibit its expression to increase the expression level of GTPBP4 in HCC cells. Finally , our findings indicated that the role of FGD5 ⁃AS1 was mediated by miR⁃873 ⁃5p GTPBP4 axis. Conclusion FGD5 ⁃AS1 promotes the proliferation , migration and invasion of HCC cells and inhibits apoptosis by regulating the miR⁃873 ⁃5p/GTPBP4 axis.