CAJ | 학술논문

目的探讨磷脂酰肌醇3激酶(PI3K)和磷酸化Akt (P-Akt)在尖锐湿疣和宫颈鳞状细胞癌发病中的作用.方法采用免疫组化和Westem印迹法检测30例尖锐湿疣、30例宫颈鳞状细胞癌及15例正常人包皮组织中PI3K和磷酸化Akt的表达,利用计算机图像采集与分析系统对免疫组化结果进行平均吸光度(A值)测定,并对免疫印迹测定结果进行灰度扫描.采用SPSS17.0软件行f检验和方差分析.结果 15例正常人皮肤中,仅表皮基底层可见PI3K及P-Akt阳性细胞；30例尖锐湿疣皮损中,PI3K及P-Akt表达增强,表皮全层均可见阳性细胞；而30例宫颈鳞状细胞癌组织中PI3K及P-Akt表达更强,明显高于尖锐湿疣,可见大量PI3K及P-Akt强阳性细胞.免疫组化图像分析结果显示,宫颈鳞状细胞癌PI3K和P-Akt表达(A值)分别为0.28±0.05和0.20±0.07,尖锐湿疣分别为0.22±0.04和0.17±0.03,正常人对照组分别为0.16±0.04和0.10±0.02,经方差分析,F值分别为44.87和20.64,P值均＜0.01.Western 印迹结果与免疫组化检测一致,宫颈鳞状细胞癌PI3K和P-Akt表达的相对灰度值分别为3.48±0.48和3.33±0.26,尖锐湿疣分别为1.99±0.11和1.96±0.11,正常人对照组分别为1.00±0.03和1.00±0.03,经方差分析,F值分别为354.83和302.33,P值均＜0.01.结论尖锐湿疣和宫颈鳞状细胞癌中PI3K/Akt信号通路被异常激活,HPV有可能通过影响PI3K和P-Akt的表达上调引起感染上皮的异常增殖.
목적 탐토린지선기순3격매(PI3K)화린산화Akt (P-Akt)재첨예습우화궁경린상세포암발병중적작용.방법 채용면역조화화Westem인적법검측30례첨예습우、30례궁경린상세포암급15례정상인포피조직중PI3K화린산화Akt적표체,이용계산궤도상채집여분석계통대면역조화결과진행평균흡광도(A치)측정,병대면역인적측정결과진행회도소묘.채용SPSS17.0연건행f검험화방차분석.결과 15례정상인피부중,부표피기저층가견PI3K급P-Akt양성세포；30례첨예습우피손중,PI3K급P-Akt표체증강,표피전층균가견양성세포；이30례궁경린상세포암조직중PI3K급P-Akt표체경강,명현고우첨예습우,가견대량PI3K급P-Akt강양성세포.면역조화도상분석결과현시,궁경린상세포암PI3K화P-Akt표체(A치)분별위0.28±0.05화0.20±0.07,첨예습우분별위0.22±0.04화0.17±0.03,정상인대조조분별위0.16±0.04화0.10±0.02,경방차분석,F치분별위44.87화20.64,P치균＜0.01.Western 인적결과여면역조화검측일치,궁경린상세포암PI3K화P-Akt표체적상대회도치분별위3.48±0.48화3.33±0.26,첨예습우분별위1.99±0.11화1.96±0.11,정상인대조조분별위1.00±0.03화1.00±0.03,경방차분석,F치분별위354.83화302.33,P치균＜0.01.결론 첨예습우화궁경린상세포암중PI3K/Akt신호통로피이상격활,HPV유가능통과영향PI3K화P-Akt적표체상조인기감염상피적이상증식.
Objective To investigate the roles of phosphatidylinositol 3 kinase (PI3K) and phosphorylated Akt (P-Akt) in the pathogenesis of cervical squamous cell carcinoma and condyloma acuminatum.Methods Immunohistochemistry and Western blot were used to detect the expressions of PI3K and P-Akt in tissue specimens from the lesions of 30 cases of cervical squamous cell carcinoma,30 cases of condyloma acuminatum and the prepuce of 15 normal human controls.The average optical density and gray scale values were calculated and analyzed by t test and F test respectively.Results The expressions of PI3K and P-Akt were observed in only the basal layer of the epidermis of control specimens,but in the whole epidermis of condyloma acuminatum tissue specimens.Cervical squamous cell carcinoma tissue specimens displayed a stronger expression of PI3K and P-Akt compared with the control and condyloma acuminatum tissue specimens.As immunohistochemistry revealed,the average absorbance value for PI3K and P-Akt was 0.28 ±0.05 and 0.20 ± 0.07 respectively in cervical squamous cell carcinoma tissue specimens,0.22 ± 0.04 and 0.17 ± 0.03 respectively in condyloma acuminatum tissue specimens,and 0.16 ± 0.04 and 0.10 ± 0.02 respectively in the control tissue specimens; significant differences were observed in the expressions of PI3K and P-Akt among the three groups of tissue specimens (F =44.87,20.64,respectively,both P ＜ 0.01 ).The results of Western blot were consistent with those of immunohistochemistry,and there was a significant difference in the gray scale value for PI3K and P-Akt between cervical squamous cell carcinoma,condyloma acuminatum and control tissue specimens (3.48 ± 0.48 vs.1.99 ± 0.11 vs.1.00 ± 0.03,F=354.83,P＜ 0.01; 3.33 ± 0.26 vs.1.96 ± 0.11 vs.1.00 ± 0.03,F=302.33,P＜ 0.01 ).Conclusions The PI3K/Akt signaling pathway is abnormally activated in condyloma acuminatum and cervical squamous cell carcinoma,and human papilloma virus may cause the abnormal proliferation of infected epithelium likely by affecting the upregnlated expression of PI3K/P-Akt.