STAT3和SOCS3蛋白在中耳胆脂瘤中的表达及意义

The Expression of STAT3 and SOCS3 Protein in the Middle Ear Cholesteatoma

目的研究信号转导和转录激活因子3(signal transducer and activator of transcription 3,STAT3)和细胞因子信号抑制因子3(suppressor of cytokine signaling 3,SOCS3)在中耳胆脂瘤中的表达及意义。方法采用免疫组织化学法检测30例中耳胆脂瘤标本与20例正常外耳道皮肤中STAT3及SOCS3蛋白的表达。结果STAT3蛋白阳性表达定位于胞浆和胞核,其在中耳胆脂瘤上皮中阳性表达率为76.7%(23/30),高于正常外耳道皮肤组的25.0%(5/20),差异有统计学意义(P<0.05);SOCS3蛋白阳性表达主要定位于胞浆,其在中耳胆脂瘤上皮的阳性表达率为33.3%(10/30),低于正常外耳道皮肤组的65.0%(13/20),差异有统计学意义(P<0.05);在30例中耳胆脂瘤上皮组织中,STAT3与SOCS3蛋白的表达呈负相关(r=-0.476,P=0.008,P<0.05)。结论STAT3和SOCS3蛋白在中耳胆脂瘤中的异常表达可能与中耳胆脂瘤上皮细胞的过度增殖和凋亡抑制相关,进而参与了胆脂瘤的发生发展。

Objective To study the expression of signal transducer and activator of transcription 3 （STAT3） and Suppressor of cytokine signaling 3（SOCS3） in the middle ear cholesteatoma epithelium ,and the possible roles of STAT3 and SOCS3 in middle ear cholesteatoma. Methods The immunohistochemical assay was used to detect expression of STAT3 and SOCS3 protein in 30 cases of middle ear cholesteatoma epithelial tissue and 20 cases of normal external auditory canal skin tissues as the control group. Results STAT3 immunoreactivity was detected in the nuclei and cytoplasm of epithelial cells. The expression rates of STAT3 in middle ear cholesteatoma epithelial tissue were 76.7% and higher than in the normal epithelium （25.0%）. The differences between the two groups were statistically significant （P%0.05）. SOCS3 immunoreactivity was detected in the cytoplasm of epithelial cells. The expression rates of SOCS3 in middle ear cholesteatoma epithelial tissue were 33.3 % and lower than in the normal epithelium （65.0 % ）. The differences were statistically significant （P〈0.05）. The expression of STAT3 and SOCS3 in the middle ear eholesteatoma had negative correlation （r = -- 0. 476, P〈0.05）. Conclusion The abnormal expression of STAT3 and SOCS3 in the middle ear cholesteatoma may be involved in hyper proliferation and anti--apoptosis of eholesteatoma cell, and play an important role in the formation and development of middle ear cholesteatoma.