[1]姜勉,董佳丽,李航,等.HBXIP蛋白表达对宫颈癌细胞的增殖能力及放射敏感性的影响[J].国际放射医学核医学杂志,2017,41(5):340-346.[doi:10.3760/cma.j.issn.1673-4114.2017.05.007]
　Jiang Mian,Dong Jiali,Li Hang,et al.Effects of HBXIP protein expression on the proliferation and radiosensitivity of cervical cancer cells[J].International Journal of Radiation Medicine and Nuclear Medicine,2017,41(5):340-346.[doi:10.3760/cma.j.issn.1673-4114.2017.05.007]
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HBXIP蛋白表达对宫颈癌细胞的增殖能力及放射敏感性的影响(/HTML)
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《国际放射医学核医学杂志》[ISSN:1673-4114/CN:12-1381/R]

卷:
41
期数:
2017年第5期
页码:
340-346
栏目:
综述
出版日期:
2017-09-25

文章信息/Info

Title:
Effects of HBXIP protein expression on the proliferation and radiosensitivity of cervical cancer cells
作者:
姜勉;  董佳丽;  李航;  樊赛军
300192 天津, 北京协和医学院中国医学科学院放射医学研究所, 天津市放射医学与分子核医学重点实验室
Author(s):
Jiang Mian;  Dong Jiali;  Li Hang;  Fan Saijun
Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Science & Peking Union Medical College, Tianjin 300192, China
关键词:
HBXIP; RNA; 小分子干扰; 宫颈肿瘤; 细胞增殖; 辐射耐受性
Keywords:
HBXIP; RNA; small interfering; Uterine cervical neoplasms; Cell proliferation; Radiation tolerance
DOI:
10.3760/cma.j.issn.1673-4114.2017.05.007
摘要:
目的 探讨用siRNA敲降乙肝病毒X蛋白结合蛋白（HBXIP）的表达对宫颈癌ME-180细胞的增殖能力及放射敏感性的影响。方法 根据不同的处理方法，分别按两种分组方式进行分组。（1）把宫颈癌ME-180细胞分为4组：空白对照组、4 Gy γ射线照射组、HBXIP-siRNA转染组以及HBXIP-siRNA+γ射线照射联合组。采用MTT和克隆形成实验法来检测细胞增殖；采用qRTPCR检测凋亡相关蛋白Bcl-2及Bid的表达；Western blot检测蛋白激酶AKT的磷酸化水平。（2）把宫颈癌ME-180细胞分为3组：空白对照组、HBXIP-siRNA单独处理组、HBXIP-siRNA和AKT共转染组。对3组细胞进行不同剂量的γ射线照射，并采用克隆形成实验方法检测细胞生长。采用Student t-test对数据进行统计学分析，P<0.05表示差异有统计学意义。结果 MTT实验和克隆形成实验结果显示，与γ射线照射组相比，HBXIP-siRNA转染+γ射线照射联合组的宫颈癌ME-180细胞增殖率明显降低（t=11.63、12.17，均P<0.01），并伴随抑凋亡蛋白Bcl-2表达的降低（t=10.88，P<0.01）和促凋亡蛋白Bid表达的增高（t=9.31，P<0.01）。γ射线照射明显上调了HBXIP蛋白的表达水平和AKT蛋白的磷酸化水平，而转染HBXIP-siRNA则抑制了γ射线照射导致的AKT磷酸化水平的升高。另外，与HBXIP-siRNA单独处理组相比，HBXIP-siRNA和AKT共转染组中HBXIP-siRNA对宫颈癌ME-180细胞增殖的影响显著降低（t=8.96，P<0.01）。结论 降低HBXIP蛋白表达可以抑制辐照诱导的AKT磷酸化水平，进而降低宫颈癌ME-180细胞的增殖能力，同时增强其放射敏感性。
Abstract:
Objective To explore the effects of (hepatitis B X-interacting protein) HBXIP downregulation on the proliferation and radiosensitivity of cervical cancer ME-180 cells. Method According to the different treatment methods, cervical cancer ME -180 cells were divided into different groups:(1)The cervical cancer ME -180 cells were divided into 4 groups:control group, 4 Gy γ ray irradiation group, HBXIP-siRNA transfection group and HBXIP-siRNA transfection+γ ray irradiation group. cervical cancer ME-180 cell proliferation was detected by MTT and clonogenic assays. The expression of Bcl-2 and Bid mRNA was detected by quantitative real-time polymerase chain reaction, and the phosphorylation of AKT protein was measured by Western blot analysis. (2)The cervical cancer ME-180 cells were divided into 3 groups:control group, HBXIP-siRNA transfection group and HBXIP-siRNA+AKT transfection group. Then the three groups of cells were irradiated with different doses of γ ray, and the cervical cancer ME-180 cell proliferation was detected by clonogenic assay. Statistical significance of the results was determined by SPSS statistical software and analyzed by Student t-test. P<0.05 were considered statistically significant. Results MTT and clonogenic assays showed that, compared with the cells irradiated alone, the cervical cancer ME-180 cells irradiated in the presence of HBXIP-siRNA had significantly decreased proliferation (t=11.63, 12.17, P<0.01). The decreased proliferation was accompanied by a decreased expression of Bcl-2 protein (t=10.88, P<0.01) and an increased expression of Bid protein (t=9.31, P<0.01). The transfection with HBXIP-siRNA inhibited the increased HBXIP protein expression and AKT phosphorylation, which were caused by radiation. The enhanced AKT expression significantly reduced the HBXIP -siRNA inhibition of cervical cancer ME-180 cell proliferation after irradiation as compared with that of the HBXIP-siRNA alone (t=8.96, P<0.01). Conclusion HBXIP down -regulation reduced the proliferation and increased the radiosensitivity of cervical cancer ME-180 cells by mediating AKT activation.

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备注/Memo

备注/Memo:
收稿日期:2017-07-02。
基金项目:国家自然科学基金（81572969）；科技部科研院所开发项目（2014EG150134）
通讯作者:樊赛军,Email:fansaijun@irm-cams.ac.cn
更新日期/Last Update: 2017-09-25