期刊文献+

子宫颈鳞状细胞癌中Aurora-A、MCM7和HPV 16 E7的表达与临床病理特征的关系 被引量:6

Expression of Aurora-A,MCM7 and HPV 16 E7 in uterine cervical squamous cell carcinoma and their relationship with clinicopathological factors
下载PDF
导出
摘要 目的探讨子宫颈鳞状细胞癌(cervical squamous cell carcinoma,CSCC)中Aurora-A激酶、微小染色体维持蛋白7(minichromosome maintenance protein 7,MCM7)和人乳头瘤病毒16型E7蛋白(human papillomavirus type 16 E7 protein,HPV 16 E7)的表达及与临床病理特征的关系。方法应用免疫组化PV 9001两步法检测子宫颈上皮内瘤变(cervical intraepithelial neoplasia,CIN)(CIN1者20例、CIN2+3者30例)、40例子宫颈鳞状细胞癌(cervical squamous cell carcinoma,CSCC)及20例慢性子宫颈炎组织中Aurora-A、MCM7及HPV 16 E7的表达,并进行定位、半定量及相互关系的分析。结果 (1)Aurora-A定位于细胞质和细胞核,MCM7蛋白阳性染色定位于细胞核,HPV 16 E7以细胞核和(或)细胞质出现棕黄色颗粒为阳性。(2)AuroraA、MCM7及HPV 16 E7在CSCC组、CIN 2+3组的表达分别高于CIN1组、慢性子宫颈炎组(P<0.008 3)。(3)子宫颈浸润癌中,Aurora-A与HPV 16 E7的表达呈正相关(P<0.001,rs=0.657),MCM7与HPV 16 E7的表达呈正相关(P<0.001,rs=0.616),Aurora-A与MCM7的表达呈正相关(P<0.001,rs=0.597)。(4)Aurora-A表达与肿瘤分化程度、临床分期及有无淋巴结转移相关(P<0.05);MCM7表达与肿瘤分化程度、临床分期相关(P<0.05);HPV 16 E7表达与患者年龄、肿瘤直径、肿瘤分化程度、临床分期及有无淋巴结转移无相关性(P>0.05)。结论 Aurora-A、MCM7及HPV 16 E7的表达随子宫颈病变进展逐渐增加,三者与子宫颈癌发生、发展密切相关,有望成为子宫颈癌早期诊断、早期治疗的生物学指标。 Purpose To explore the expression of Aurora kinase A (Aurora-A), minichromosome maintenance protein 7 (MCM7) and human papillomavirus type 16 E7 protein (HPV 16 E7) in uterine cervical squamous cell carcinoma (CSCC) and to investigate their relationship with clinicopathological factors. Methods Immunohistochemical method was employed on 20 cases of low-grade cervical intraepithelial neoplasia (CIN1) , 30 cases of high-grade cervical intraepithelial neoplasia (CIN2+3), 40 cases of CSCC, and 20 ca-ses of chronic cervicitis. Results (1) Aurora-A localized in the cytoplasm and nucleus. MCM7 protein positive staining localized in the nucleus. In the nucleus, and (or) the cytoplasm appeared brown particles positive for HPV 16 E7. (2) The expression of Aurora-A, MCM7 and HPV 16 E7 were higher in the group of CIN2+3 and CSCC than that in the group of chronic cervicitis or CIN1 ( P〈0. 0083). (3) In cervical cancer, the expression of Aurora-A, HPV 16 E7 showed positive correlation (P〈0. 001, rs =0. 657). The expression of MCM7, HPV 16 E7 showed positive correlation (P〈0. 001, rs =0. 616). The expression of Aurora-A, MCM7 showed positive correlation (P〈0. 001, rs =0. 597). (4) Aurora-A expression levels was associated with tumor cell differentiation, clinical stage and lymph node metastasis (P〈0. 05). MCM7 expression levels was associated with tumor cell differentiation and clinical stage (P〈0. 05). HPV 16 E7 expression had no correlation with patient age, tumor size, tumor differentiation, clinical stage and lymph node metastasis (P〉0. 05). Conclusion Aurora-A, MCM7 and HPV 16 E7 expression are gradually increased with disease progres-sion, and closely related to the occurrence and development of cervical cancer, they are expected to be early diagnosis, early treatment of biological indicators of cervical cancer.
出处 《临床与实验病理学杂志》 CAS CSCD 北大核心 2015年第5期497-501,共5页 Chinese Journal of Clinical and Experimental Pathology
基金 江苏省妇幼保健科研项目(F201401)
关键词 子宫颈肿瘤 鳞状细胞癌 AURORA-A MCM7 HPV 16 E7 免疫组织化学 cervical neoplasm squamous cell carcinoma Aurora-A immunohistochemistry
  • 相关文献

参考文献4

二级参考文献53

  • 1Xiao Xia Wang,Rong Liu,Shun Qian Jin,Fei Yue Fan,Qi Min Zhan.Overexpression of Aurora-A kinase promotes tumor cell proliferation and inhibits apoptosis in esophageal squamous cell carcinoma cell line[J].Cell Research,2006,16(4):356-366. 被引量:24
  • 2Yu Z, Feng D, Liang C. Pairwise interactions of the six human MCM protein subunits[J]. J Mol Biol, 2004, 340 ( 5 ) : 1197- 1206.
  • 3You Z, Ishimi Y, Masai H, et al. Roles of MCM7 and MCM4 subunits in the DNA helicase activity of the mouse MCM4/6/7 complex[J]. J Biol Chem, 2002, 277(45): 42471- 42479.
  • 4Lei M, Tye BK. Initiating DNA synthesis: from recruiting to activating the MCM complex [J]. J Cell Sci, 2001, 114 (Pt 8): 1447-1454.
  • 5Shechter D, Gautier J. ATM and ATR check in on origins: a dynamic model for origin selection and activation[J]. Cell Cycle, 2005, 4(2): 235-238.
  • 6Todorov IT, Attaran A, Kearsey SE. BM28, a human member of the MCM2-3-5 family, is displaced from chromatin during DNA replication[J]. J Cell Biol, 1995, 129(6): 1433-1445.
  • 7Labib K, Tercero JA, Diffley JF. Uninterrupted MCM2-7 function required for DNA replication fork progression[J]. Science, 2000, 288(5471): 1643-1647.
  • 8Madine MA, Swietlik M, Pelizon C, et al. The role of the MCM, ORC, and CDC6 proteins in determining flue replication competence of chromatin on quiescent cell [J]. J Struct Biol, 2000, 129(2-3): 198-210.
  • 9Bailis JM, Luche DD, Hunter T, et al. Minichromosome maintenance proteins interact with checkpoint and recombination proteins to promote S-phase genome stability[J]. Mol Cell Biol, 2008, 28(5): 1724-1738.
  • 10Forsburg SL. The MCM helicase: linking checkpoints to the replication fork[J]. Biochem Soc Trans, 2008, 36(Pt 1): 114-119.

共引文献25

同被引文献48

引证文献6

二级引证文献10

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部