Shanghai Journal of Stomatology ›› 2017, Vol. 26 ›› Issue (4): 389-394.doi: 10.19439/j.sjos.2017.04.008

• Orignal Article • Previous Articles     Next Articles

Effect of HBXIP on biological function and PI3K/Akt signaling pathway of adenoid cystic carcinoma cell line ACC-M

MENG Xue1, QI Xiao-yu2, WANG Qiu-xu1, LIU Wei-xian1   

  1. 1.Department of Oral and Maxillofacial Surgery, Shengjing Hospital Affiliated to China Medical University. Shenyang 110004;
    2.Department of Stomatology, Liaoning Provincial Tiefa Coal Group General Hospital. Tieling 112000, Liaoning Province, China
  • Received:2017-02-04 Revised:2017-03-27 Online:2017-08-25 Published:2017-09-01

Abstract: To study the effect of hepatitis B virus X protein binding protein (HBXIP) on proliferation, migration and invasion of adenoid cystic carcinoma cell line ACC-M, and the possible mechanism of PI3K/Akt signaling pathway. METHODS: HBXIP plasmid was transfected into ACC-M. The cells were divided into experimental group (transfected with plasmid pEGFP-N1-HBXIP) control group (non-transfected group) and blank control group (vector group, pEGFP-N1). RT-PCR was used to detect the expression HBXIP in ACC-M; MTT assay, transwell chamber experiments and scratches over the proliferation of HBXIP were utilized individually to evaluate the influence of HBXIP on ACC-M expression, migration and invasion; Western blotting was used to detect the protein expression of Akt, p-Akt, PI3K, p-PI3K and S100A4 after overexpression of HBXIP. Statistical analysis was performed using SPSS 18.0 software package. RESULTS: MTT results showed that the number of surviving cells of experimental group was significantly higher than the control group (P<0.05); Scratch test results showed that the cell mobility of the experimental group was significantly higher than the control group (P<0.01); Transwell chamber experiments showed that the number of cell invasion of the experimental group was significantly higher than the control group (P<0.01); Western blotting results showed that compared with the control group, the expression of p-Akt, p-PI3K and S100A4 in the experimental group with overexpressed HBXIP was relatively increased. CONCLUSIONS: Overexpression of HBXIP gene promotes ACC-M proliferation, invasion and migration. Further, ACC-M proliferation, invasion and migration may be promoted by increased Akt, PI3K phosphorylation and S100A4 protein expression.

Key words: Hepatitis B X-interacting protein, ACC-M, Salivary gland, Biological functions, PI3K/Akt signaling pathway, S100A4

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