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目的探讨尖锐湿疣(CA)皮损角质形成细胞中细胞因子信号转导JAK/STAT通路负调控蛋白细胞因子信号抑制剂-1(SOCS1)和活化STAT的蛋白抑制剂-1(PIAS1)的表达。方法采用SP免疫组化染色技术检测40例CA患者皮损、20例宫颈癌和20例正常人皮肤(包皮)中SOCS1和PIAS1的表达及分布。结果①CA患者皮损中SOCS1和PIAS1的表达阳性细胞分布主要位于棘细胞层,为棕黄着色,阳性反应定位胞质;宫颈鳞状细胞癌亦为胞质阳性表达,棕黄着色,呈弥漫性分布;而正常包皮少数阳性着色主要定位于基底层细胞的胞质,呈浅黄着色。②CA皮损中SOCS1和PIAS1的表达阳性率分别为85%和80%,高于在正常人上皮中的表达(阳性率分别为30%和35%),两组比较差异均有统计学意义(前者χ~2=18.15,P<0.01;后者χ~2=11.87,P<0.01);宫颈癌中SOCS1和PIAS1的表达阳性率分别为90%和85%,虽较CA有升高,但两者比较差异均无统计学意义(两者均P>0.05)。③CA中SOCS1与PIAS1的表达无显著相关性(r_s=0.14,P>0.05)。结论CA皮损中可能通过细胞因子信号转导负调控蛋白SOCS1和PIAS1在角质形成细胞过度增殖或恶性转化过程中起调控作用。
Objective To investigate the expression of cytokine signaling JAK / STAT pathway negative regulatory protein cytokine signaling inhibitor-1 (SOCS1) and activation of STAT protein inhibitor-1 (PIAS1) in keratinocytes of condyloma acuminatum (CA) Methods SP immunohistochemical staining was used to detect the expression and distribution of SOCS1 and PIAS1 in 40 cases of CA lesions, 20 cases of cervical cancer and 20 cases of normal skin (foreskin). Results ① The positive cells of SOCS1 and PIAS1 in the lesional lesions of CA were mainly located in the spine cell layer, which was brown-yellow and positively localized cytoplasm. Cervical squamous cell carcinoma was also positive for cytoplasm, brown-yellow and diffuse Distribution; while a small number of normal foreskin positive staining mainly located in the cytoplasm of basal cells, pale yellow. ② The positive rates of SOCS1 and PIAS1 expression in CA lesions were 85% and 80%, respectively, which were higher than those in normal human epithelium (positive rates were 30% and 35%, respectively). There were significant differences between the two groups The former positive rate of SOCS1 and PIAS1 in cervical cancer was 90% and 85%, respectively, although it was higher than that of CA There was no significant difference between the two groups (both P> 0.05). There was no significant correlation between SOCS1 and PIAS1 expression in CA (r_s = 0.14, P> 0.05). Conclusion The CA lesions may play a regulatory role in the process of keratinocyte hyperproliferation or malignant transformation through the negative regulatory proteins of cytokine signaling SOCS1 and PIAS1.