Meng Xue, Qi Xiao-Yu, Wang Qiu-Xu, Liu Wei-Xian
Department of Oral and Maxillofacial Surgery, Shengjing Hospital Affiliated to China Medical University. Shenyang 110004. E-mail:
Shanghai Kou Qiang Yi Xue. 2017 Aug;26(4):389-394.
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.
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.
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.
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.
研究乙型肝炎病毒X蛋白结合蛋白（HBXIP）对腺样囊性癌细胞系ACC-M增殖、迁移和侵袭的影响以及PI3K/Akt信号通路的可能机制。
将HBXIP质粒转染至ACC-M细胞。细胞分为实验组（转染质粒pEGFP-N1-HBXIP）、对照组（未转染组）和空白对照组（载体组，pEGFP-N1）。采用RT-PCR检测ACC-M中HBXIP的表达；分别利用MTT法、Transwell小室实验和划痕实验评估HBXIP对ACC-M增殖、迁移和侵袭的影响；采用蛋白质免疫印迹法检测过表达HBXIP后Akt、p-Akt、PI3K、p-PI3K和S100A4的蛋白表达。使用SPSS 18.0软件包进行统计学分析。
MTT结果显示，实验组存活细胞数显著高于对照组（P<0.05）；划痕实验结果显示，实验组细胞迁移能力显著高于对照组（P<0.01）；Transwell小室实验显示，实验组细胞侵袭数显著高于对照组（P<0.01）；蛋白质免疫印迹结果显示，与对照组相比，过表达HBXIP的实验组中p-Akt、p-PI3K和S100A4的表达相对增加。
HBXIP基因过表达促进ACC-M的增殖、侵袭和迁移。此外，Akt、PI3K磷酸化及S100A4蛋白表达增加可能促进ACC-M的增殖、侵袭和迁移。
