国际妇产科学杂志

国际妇产科学杂志 ›› 2011, Vol. 38 ›› Issue (4): 332-334.

• 论著 • 上一篇    下一篇

FHIT基因、HPV16E6的表达与宫颈鳞癌发病的相关性研究

李惠新,李 敏,王小娇   

  1. 730030 兰州大学第二医院妇产科(李惠新,王小娇);兰州大学病理学与病理生理学教研室(李敏)
  • 收稿日期:1900-01-01 修回日期:1900-01-01 出版日期:2011-08-15 发布日期:2011-08-15
  • 通讯作者: 李惠新

Expression of FHIT， HPV16E6 and Its Correlation with Cervical Squamous Carcinoma

LI Hui-xin， LI Min， WANG Xiao-jiao   

  1. Department of Obstetrics and Gynecology， Second Hospital of Lanzhou University， Lanzhou 730030， China （LI Hui-xin， WANG Xiao-jiao）; Department of Pathology and Pathophysiology， Lanzhou University， Lanzhou 730000， China （LI Min）
  • Received:1900-01-01 Revised:1900-01-01 Published:2011-08-15 Online:2011-08-15
  • Contact: LI Hui-xin

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摘要： 目的：探讨抑癌基因脆性组氨酸三联（fragile histine triad，FHIT）基因、人乳头瘤病毒16E6（HPV16E6）蛋白在宫颈鳞癌中的表达及其相互关系。方法：应用免疫组织化学链霉菌抗生物素蛋白－过氧化物酶连接（SP）法观察40例宫颈鳞癌、30例宫颈上皮内瘤样病变（CIN）和30例正常宫颈组织中FHIT基因、HPV16E6的表达。结果：FHIT基因在正常宫颈组织、CIN和宫颈鳞癌组织中的阳性表达率分别为96.7%，66.7%和30.0%，各组间阳性等级表达比较差异有统计学意义（χ2=43.595，P＜0.001）。FHIT基因阳性表达在宫颈鳞癌病理分级、临床分期中的比较，差异无统计学意义（χ2分别为3.378和3.315，均P＞0.05）。HPV16E6在正常宫颈组织、CIN和宫颈鳞癌组织中的阳性表达率分别为13.3%，53.3%和82.5%，各组间阳性等级表达比较差异有统计学意义（χ2=32.538，P＜0.001）。HPV16E6蛋白阳性表达在宫颈鳞癌病理分级、临床分期中的比较，差异无统计学意义（χ2分别为0.231和1.399，均P＞0.05）。结论：宫颈鳞癌中FHIT基因表达减少或缺失，以及HPV16E6的高检出率，提示二者在宫颈鳞癌的发生发展中起重要作用，可能是宫颈鳞癌发病机制之一。通过对FHIT基因和HPV16E6蛋白的致病机制以及相互影响的研究，有助于揭示宫颈癌发病机制，二者有可能用于临床宫颈癌诊断、

关键词: 宫颈肿瘤, 人乳头瘤病毒16, 基因, 肿瘤抑制, 免疫组织化学, FHIT基因

Abstract: Objective: To study tumor suppressor gene——fragile histidine triad（FHIT）， human papillomavirus16E6（HPV16E6） expression and their significance in cervical squamous carcinomas（CSC）. To study the correlation between FHIT， HPV16E6 in CSC. Methods: Immunohistochemical staining for FHIT， HPV16E6 were performed by SP methods in 40 cases of CSC， 30 cases of cervical intraepithelial neoplasias（CIN）， and 30 cases of normal cervical epithelium. Results: The express of FHIT in 96.7% of normal cervical epithelium， 66.7% of CIN and 30.0% of the CSC， FHIT expression showed significant statistical difference（χ2=43.595， P＜0.001）. The expression of FHIT in the degree of differentiation and clinic stages of CSC indicates no statistical difference （χ2=3.378， χ2=3.315， P＞0.05）. The expression of HPV16E6 in 13.3% of normal cervical epithelium， 53.3% of CINs， and 82.5% of the CSC， HPV16E6 expression showed significant statistical difference（χ2=32.538， P＜0.001）. The expression of HPV16E6 in the degree of differentiation and clinic stages of CSC were observed no statistical difference （χ2=0.231， χ2=1.399， P＞0.05）. Conclusions: The FHIT gene expression deletion and the high detection rate of HPV16E6 in the CSC indicate that these two factors play an important role in the CSC development mechanism. The infection of HPV16-E6 and the FHIT gene deletion might be the one of the CSC pathogenesises（or might be the causes of CSC）. The results of this study that FHIT gene and HPV16E6 biological effects on CSC development and their interaction in CSC could help reveal the pathogenesis of CSC. These two factors could be the potential CSC clinical diagnosis indicator and useful in CSC precaution and gene therapy.

Key words: Uterine cervical neoplasms, Human papillomavirus 16, Genes, tumor suppressor, Immunohistochemistry, FHIT gene