HBXIP对腺样囊性癌细胞株ACC-M生物学功能及PI3K/Akt信号通路的影响

doi:10.19439/j.sjos.2017.04.008

上海口腔医学 ›› 2017, Vol. 26 ›› Issue (4): 389-394.doi: 10.19439/j.sjos.2017.04.008

HBXIP对腺样囊性癌细胞株ACC-M生物学功能及PI3K/Akt信号通路的影响

孟雪^{1, *}, 齐晓宇^{2, *}, 王秋旭¹, 刘维贤¹

1.中国医科大学附属盛京医院口腔颌面外科,辽宁沈阳 110004；
2.辽宁省铁法煤业集团总医院口腔科,辽宁铁岭 112000

收稿日期:2017-02-04 修回日期:2017-03-27 出版日期:2017-08-25 发布日期:2017-09-01
通讯作者: 刘维贤,E-mail：liuwx@sj-hospital.org
作者简介:孟雪（1986-）,女,硕士,E-mail：cmumengxue@126.com;齐晓宇（1984-）,男,博士,E-mail：geshiyayi@126.com。*并列第一作者
基金资助:
高等学校博士点基金课题（20132104110012）

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.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

摘要/Abstract

摘要： 目的研究乙肝病毒X蛋白结合蛋白（hepatitis B X-interacting protein, HBXIP）对唾液腺腺样囊性癌肺高转移细胞株（ACC-M）增殖、迁移和侵袭的影响,及其对PI3K/Akt信号通路的影响。方法将HBXIP质粒转染到ACC-M中,将细胞分为实验组（转染pEGFP-N1-HBXIP质粒）、对照组1（未转染组）和对照组2（vector组,pEGFP-N1）。采用RT-PCR检测HBXIP在ACC-M中的表达;采用MTT实验、Transwell小室实验和划痕实验检测HBXIP过表达对ACC-M的增殖、迁移和侵袭的影响;Western印迹法检测HBXIP过表达对Akt、p-Akt、PI3K、p-PI3K及S100A4蛋白表达量的影响。采用SPSS18.0软件包对数据进行统计学分析。结果MTT实验结果显示,实验组中存活的细胞数显著高于对照组（P<0.05）;划痕实验结果显示,实验组细胞迁移率显著高于对照组（P<0.01）;Transwell小室实验结果显示,实验组细胞侵袭个数显著高于对照组（P<0.01）;Western印迹法结果显示,相对于对照组,实验组随着HBXIP过表达,p-Akt、p-PI3K及S100A4表达量相对增高。结论HBXIP基因过表达ACC-M增殖、迁移和侵袭具有影响,可能通过促进Akt、PI3K磷酸化及S100A4蛋白表达量增加,促进ACC-M的增殖、迁移和侵袭。

关键词: 乙肝病毒X蛋白结合蛋白, 唾液腺腺样囊性癌肺高转移细胞株, 唾液腺, 生物学功能, PI3K/Akt信号通路, S100A4

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

中图分类号:

R782.7

孟雪, 齐晓宇, 王秋旭, 刘维贤. HBXIP对腺样囊性癌细胞株ACC-M生物学功能及PI3K/Akt信号通路的影响[J]. 上海口腔医学, 2017, 26(4): 389-394.

MENG Xue, QI Xiao-yu, WANG Qiu-xu, LIU Wei-xian. Effect of HBXIP on biological function and PI3K/Akt signaling pathway of adenoid cystic carcinoma cell line ACC-M[J]. Shanghai Journal of Stomatology, 2017, 26(4): 389-394.

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HBXIP对腺样囊性癌细胞株ACC-M生物学功能及PI3K/Akt信号通路的影响

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

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