客家人非小细胞肺癌HPV16型感染与p27^(Kip1)蛋白表达的关系

Relationship between HPV16 infection and p27^(Kip1) protein expression in non-small cell lung cancer of hakka

目的:探讨客家人非小细胞肺癌(non-small cell lung cancer,NSCLC)HPV16型(HPV-16)感染与p27^(Kip1)蛋白表达的关系。方法:收集2004年3月至2008年12月梅州市人民医院(中山大学附属梅州医院)外科手术切除并经病理确诊的43例NSCLC标本,其中鳞癌20例,腺癌23例,另选取同一时期肺良性病变27例作为对照组。应用免疫组织化学技术(SABC法)检测以上标本中HPV-16和p27^(Kip1)蛋白的表达情况,并用Spearman等级相关检验对两种蛋白在NSCLC中的表达进行相关性分析。结果:HPV-16在NSCLC组织中细胞质阳性率(39.5%)高于肺良性病变的细胞质表达(7.4%),差异有统计学意义(P<0.01);p27^(Kip1)蛋白表达可见于NSCLC组织细胞核或细胞质,细胞核表达阳性率为9.3%,显著低于肺良性病变组织细胞核表达(44.4%,P<0.05);细胞质表达丰富,阳性率为48.8%,显著高于肺良性病变组织细胞质表达(7.4%,P<0.05);p27^(Kip1)蛋白细胞核表达与细胞质表达呈负相关,差异有统计学意义(P>0.05);HPV感染和p27^(Kip1)蛋白在NSCLC组织中表达的相关性分析发现HPV-16在NSCLC中的表达与p27^(Kip1)蛋白细胞质表达呈正相关,差异有统计学意义(P<0.05),与p27^(Kip1)蛋白细胞核表达有负相关的趋势(P=0.094)。结论:从HPV,p27^(Kip1)在NSCLC组织和肺良性病变表达的结果中,推测HPV-16可能通过调控p27^(Kip1)蛋白从细胞核泄漏到细胞质,并滞留在细胞质,使p27^(Kip1)蛋白不能发挥其在细胞核中的抑瘤作用,进而促进NSCLC的发生发展。

Objective: To explore the relationship between the expression of human papillomavirus type16 (HPV-16) infection and p27^Kip1 in non-small cell lung cancer (NSCLC) of hakka. Methods: We collected 43 cases of NSCLC specimens by surgical removal and pathological diagnosis from Meizhou People’s Hospital (Meizhou Hospital Affiliated to Sun Yat-sen University) in March 2004 to December 2008, including 20 cases squamous carcinoma and 23 cases of adenocarcinoma;27 cases of lung benign lesions during the same period were selected as a control group. The expression of HPV-16 and p27^Kip1 in the above specimens was detected by immunohistochemistry (SABC), and the correlation analysis of two proteins in NSCLC was conducted with Spearman rank correlation test. Results: The cytoplasmic positive rate (39.5%) of HPV-16 in NSCLC tissues was higher than that in lung benign lesions (7.4%), and statistical analysis showed significant difference (P<0.01);p27^Kip1 protein expression was observed in NSCLC tissue cell nucleus or cytoplasm, and the positive rate of cell nuclear expression was 9.3%, which was significantly lower than that of lung benign lesions (44.4%;P<0.05);and cytoplasm expression was abundant and positive rate was 48.8%, which was significantly higher than that of pulmonary benign lesions cytoplasm expression (7.4%, P<0.05);p27^Kip1 protein nuclear expression was negatively correlated with cytoplasmic expression, which was statistically significant. HPV-16 expression and cytoplasm p27^Kip1 protein expression in NSCLC were positively correlated, with statistical significance (P<0.05) and p27^Kip1 protein nucleus expression had a tendency of negative correlation (P=0.094). Conclusion: From the results of HPV-16 and p27^Kip1 expression in NSCLC tissues and pulmonary benign lesions, we speculate that HPV-16 may leakage from nucleus to cytoplasm and stranded in cytoplasm through regulating p27^Kip1 protein, making p27^Kip1 protein not play its role in nuclei of tumor suppression, thus promoting the development of NSCLC.