Mechanism About HBX And PI3K/Akt Signaling Pathway In Salivary Adenoid Cystic Carcinoma

Objectiv: This study is to explore the expression of HBX,phosphatidylinositol3-kinase (PI3K) and its downstream serine threonine kinase (Akt) in adenoid cystic carcinoma and adenoid cystic carcinoma cell encoded with HBX, as well as how HBX impacts on PI3K/Akt signaling pathway. Methods:Restructuring adenoid cystic carcinoma cells encoded with HBX genethrough transgenosis techniques, and then to explore the influence of HBX on signaling pathway of PI3K/Akt through cell scarification, cell culture and Western blot techniques. In adddition, the effects of PD98059and EGF on ACC-M and ACC-M/HBX were observed, respectively, Finally, the expression of HBX,PI3K and Akt were detected.Results:1. Transfection rate of HBX gene was73.16%instantly using electric transfection technique, stable transient cell clone could not be obtained using screening of G418in the end.2. P13K and Akt were expressed in ACC-M cells except of HBX. Reversely in recombined ACC-M/HBX cells. Following dealting with PD98059as MEK/ERK signal transduction pathway inhibitor, expression of P13K and Akt in ACC-M/HBX were the same level as PI3K/Akt in ACC-M cells.3. ACC-M cells showed higher healing rate than ACC-M/HBX cells through cell wound scratch assay technique, there was statistically difference.Conclusions:1. PI3K/Akt signaling pathway may affected and degraded by HBX through MEK/ERK signaling pathway.2. MEK/ERK signaling pathway is the important pathway of HBX, which may be linked to PI3K/Akt signaling pathway.3.Epidermal growth factor (EFG) has no significant biological activity effects on ACC-M/HBX cell. By comparison, PD98059can inhibits the biological activity of ACC-M/HBX.