论文部分内容阅读
目的探讨髓样分化因子88(MyD88)和转录激活因子3(STAT3)在肝细胞癌(HCC)组织中的表达及其生物学意义。方法采用免疫组化方法检测MyD88和STAT3在82例肝癌组织及其对应的癌旁肝组织中的表达水平。结合肝癌临床病理指标分析它们的相关性。结果 MyD88和STAT3蛋白在癌组织中的阳性表达率分别为67.1%(55/82)和69.5%(57/82),高于癌旁肝组织中的11.0%(9/82)和8.5%(7/82),差异均具有统计学意义(P<0.05)。在肝癌组织中MyD88与STAT3的阳性表达呈正相关(r=0.578,P=0.002)。MyD88和STAT3表达与HCC患者的性别、癌的分化程度、有无HBV感染和肝硬化有关;上述4指标分组间差异具有显著性(P<0.05)。而与HCC肿瘤大小及有无静脉浸润无关;该2指标分组间差异无显著性(P>0.05)。结论 MyD88和STAT3表达上调,导致肝癌细胞增殖和免疫逃逸是肝癌发生发展的重要分子机制。
Objective To investigate the expression and biological significance of myeloid differentiation factor 88 (MyD88) and transcriptional activator 3 (STAT3) in hepatocellular carcinoma (HCC). Methods Immunohistochemistry was used to detect the expression of MyD88 and STAT3 in 82 cases of hepatocellular carcinoma and their corresponding paracancerous liver tissues. Combined with clinical and pathological indicators of liver cancer their correlation. Results The positive expression rates of MyD88 and STAT3 in cancer tissues were 67.1% (55/82) and 69.5% (57/82), respectively, which were higher than those in 11% (9/82) and 8.5% 7/82), the differences were statistically significant (P <0.05). The positive expression of MyD88 and STAT3 in HCC tissues was positively correlated (r = 0.578, P = 0.002). The expression of MyD88 and STAT3 were related to the gender, the degree of cancer differentiation, HBV infection and cirrhosis in HCC patients. There was significant difference among the above 4 indicators (P <0.05). But not with the size of HCC tumor and the presence or absence of venous invasion. There was no significant difference between the two groups (P> 0.05). Conclusion MyD88 and STAT3 are up-regulated, resulting in the proliferation and immune escape of hepatocellular carcinoma (HCC), which are important molecular mechanisms for the development of HCC.