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目的辣椒素受体-1(VR1)主要表达在神经元细胞上,但也参与肿瘤形成过程。为了阐明其在人类原发性肝细胞癌形成过程中的作用,该实验检测VR1在原发性肝细胞癌样本中癌组织和非癌组织中的表达。方法收集62例原发性肝细胞癌病例的病理标本和临床资料。用原位杂交和免疫组织化学实验来检验VR1受体的表达及其与临床病理特征之间的关系。结果(1)原位杂交实验结果:VR1mRNA在肝癌的癌组织和非癌组织中高表达的百分率为40.0%(6/15)、60.0%(9/15)。(2)免疫组织化学实验结果:62例肝癌的非癌组织中,VR1表达显著多在肝硬化组织中[31/38(81.6%)];在肝癌组织中VR1受体的高表达30例30/62(48.4%)。(3)临床病理评估结果:VR1受体的高表达与肿瘤细胞分化程度(P=0.001)二者之间存在显著的相关性。结论辣椒素受体-1在原发性肝细胞癌的非癌组织和癌组织中均有高表达,VR1受体的高表达与肝癌临床病理特征的肿瘤细胞分化程度二者之间存在显著性的相关。本组结果表明:VR1可能在原发性肝细胞癌的发生过程中起作用。
Purpose Capsaicin receptor-1 (VR1) is predominantly expressed on neuronal cells but is also involved in tumorigenesis. To clarify its role in the development of human primary hepatocellular carcinoma, the experiment examined the expression of VR1 in cancerous and non-cancerous tissues of primary hepatocellular carcinoma samples. Methods The pathological specimens and clinical data of 62 cases of primary hepatocellular carcinoma were collected. In situ hybridization and immunohistochemistry were used to test the expression of VR1 receptor and its relationship with clinicopathological features. Results (1) In situ hybridization results: The percentage of VR1 mRNA overexpressed in HCC tissues was 40.0% (6/15) and 60.0% (9/15), respectively. (2) Immunohistochemistry results: In 62 cases of non-cancerous liver cancer, the expression of VR1 was significantly higher in cirrhotic tissues [31/38 (81.6%)]; the high expression of VR1 receptors in hepatocellular carcinoma 30 cases /62(48.4%). (3) The results of clinicopathological evaluation showed that there was a significant correlation between the high expression of VR1 receptor and the degree of tumor cell differentiation (P = 0.001). Conclusions Capsaicin receptor-1 is overexpressed in non-cancerous tissues and cancerous tissues of primary hepatocellular carcinoma. There is a significant difference between the high expression of VR1 receptor and the differentiation degree of tumor cells in clinicopathological features of hepatocellular carcinoma Related. This group of results show that: VR1 may play a role in the pathogenesis of primary hepatocellular carcinoma.