摘要
目的探讨人乳头状瘤病毒(HPV)感染在非小细胞肺癌(NSCLC)发生中的病因学意义,并初步分析HPV感染与低氧诱导因子-1α(HIF-1α)和血管内皮生长因子(VEGF)蛋白表达之间的关系。方法用免疫组化法检测60例NSCLC及20例肺良性病变组织中HIF-1α和VEGF蛋白表达,用PCR法选用HPV16、18型特异性引物检测两组中HPV DNA的表达。结果 1)NSCLC组HPV DNA积分吸光度比值为0.6046±0.0224,显著高于肺良性病变组的0.0275±0.1230(P<0.05)。2)NSCLC组HIF-1α和VEGF蛋白的平均吸光度值分别为0.2548±0.0219和0.2051±0.0321,均显著高于肺良性病变组(0.0826±0.0150和0.0726±0.0227)(P<0.05)。3)NSCLC中HIF-1α的表达率与VEGF呈正相关(P<0.05)。4)NSCLC中HPV(+)组VEGF的表达率为56.0%,显著高于HPV(-)组的28.6%(P<0.05)。结论 HPV感染可能是NSCLC发生的病因学因素之一;HPV感染可能通过上调VEGF的表达,促进肺癌的发生发展。
Objective To investigate the etiological role of human papillomavirus (HPV) infection in the carcinogenesis of non-small cell lung cancer(NSCLC) and to discuss the possible relationship between HPV infection and HIF-1 α, VEGF expression. Methods By using immunohistochemistry, the expressions of HIF-1α and VEGF protein were detected in 60 cases of NSCLC tissues and 20 cases of lung benign diseases tissues. PCR was employed to detect the expression of HPV16/18 DNA. Results 1 ) The HPV DNA expression was 0. 6046 ±0. 0224 in NSCLC group which significantly higher than 0. 0275±0. 1230 in the benign diseases group (P 〈0. 05). 2)The HIF-1α protein and VEGF protein expressions were 0. 2548 ±0. 0219 and 0. 2051 ±0. 0321 respectively in NSCLC, significantly higher than that in the benign diseases group (0. 0826±0. 0150 and 0. 0726 ±0. 0227) (P 〈0. 05). 3)The expression rate of HIF-1α was significantly correlated with VEGF in NSCLC (P 〈 0. 05 ). 4)The positive expression rate of VEGF was significantly higher in HPV DNA positive group (56. 0% ) than that in HPV DNA negative group(28. 6%,P 〈 0. 05) in NSCLC. Conclusions HPV infection may be one of the etiological factors in the carcinogenesis of NSCLC. HPV infection increases VEGF expression, promotes the occurrence and development of NSCLC.
出处
《基础医学与临床》
CSCD
北大核心
2014年第8期1065-1070,共6页
Basic and Clinical Medicine
基金
秦皇岛市科技支撑计划(2012023A135)