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目的:研究hTERC基因与宫颈癌前病变及宫颈癌发生发展的关系。方法:选择在我院接受宫颈病理活检的受试者120例进行研究,包括正常宫颈组织和炎症宫颈组织45例、宫颈上皮内瘤变组织37例、宫颈癌组织38例,测定宫颈组织中hTERC基因表达量、癌基因表达量以及侵袭分子的含量。结果:宫颈癌组织中hTERC的绿色信号拷贝数、红色信号拷贝数明显高于宫颈上皮内瘤变组织和正常宫颈组织,hTERT、hTP的含量与宫颈上皮内瘤变组织和正常宫颈组织比较无差异;宫颈癌组织中p63、TNFAIP8、SRX、P459arom、Piwil2所编码蛋白的含量以及RbAp48、Furin、MT1-MMP、TGF-β1、FoxM1、uPA、tPA的含量明显高于宫颈上皮内瘤变组织和正常宫颈组织;hTERC高表达的宫颈癌组织中p63、TNFAIP8、SRX、P459arom、Piwil2所编码蛋白的含量以及RbAp48、Furin、MT1-MMP、TGF-β1、FoxM1、uPA、tPA的含量明显高于hTERC低表达的宫颈癌组织。结论:端粒酶的活化、hTERC表达量的增加参与宫颈癌前病变及宫颈癌的发生发展,hTERC能够激活癌基因的表达、增加侵袭分子的生成。
Objective: To investigate the relationship between hTERC gene and cervical precancerous lesions and cervical cancer. Methods: A total of 120 subjects with cervical biopsy undergoing cervical biopsy in our hospital were enrolled in the study, including 45 cases of normal cervical tissue and inflammatory cervical tissue, 37 cases of cervical intraepithelial neoplasia and 38 cases of cervical cancer. The hTERC Gene expression, oncogene expression and invasion molecule content. Results: The green signal copy number and red signal copy number of hTERC in cervical cancer tissues were significantly higher than that in cervical intraepithelial neoplasia tissues and normal cervical tissues. The content of hTERT and hTP in cervical cancer tissues showed no difference with cervical intraepithelial neoplasia tissues and normal cervical tissues The content of protein encoded by p63, TNFAIP8, SRX, P459arom and Piwil2 and the content of RbAp48, Furin, MT1-MMP, TGF-β1, FoxM1, uPA and tPA in cervical cancer tissues were significantly higher than those in cervical intraepithelial neoplasia tissues The content of protein encoded by p63, TNFAIP8, SRX, P459arom and Piwil2, as well as the contents of RbAp48, Furin, MT1-MMP, TGF-β1, FoxM1, uPA and tPA in cervical cancer tissues with high expression of hTERC were significantly higher than those with low hTERC Expressed cervical cancer tissue. Conclusion: The activation of telomerase and the increase of hTERC expression are involved in the development of cervical precancerous lesions and cervical cancer. HTERC can activate the expression of oncogenes and increase the generation of invasive molecules.