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为研究EDAG在人乳头状甲状腺癌病人组织中的表达及在乳头状甲状腺癌细胞中的作用,利用免疫组化检测31例乳头状甲状腺癌癌组织及癌旁组织中EDAG蛋白的表达,并进行数据分析.包装EDAG敲低慢病毒颗粒,感染乳头状甲状腺癌细胞系K1,建立EDAG敲低稳定细胞株,检测EDAG敲低对细胞增殖、克隆形成、周期和凋亡的影响.结果显示,EDAG蛋白在乳头状甲状腺癌癌组织中异常高表达,而在对应癌旁组织极低表达或不表达.建立稳定敲低EDAG的K1细胞株,敲低效果达到约96%,敲低EDAG后细胞增殖变缓,倍增时间由18.49±0.19 h变为19.47±0.11 h,且克隆形成能力下降,G0/G1期比例升高,无血清培养时凋亡增多.本文报道了EDAG在乳头状甲状腺癌病人中高表达,且敲低甲状腺癌细胞系K1中内源EDAG抑制细胞增殖,降低细胞克隆形成能力,G0/G1期增多,凋亡升高,提示EDAG异常高表达可能在甲状腺癌发生发展中具有重要作用.
To investigate the expression of EDAG in human papillary thyroid carcinoma tissues and its role in papillary thyroid carcinoma cells, immunohistochemistry was used to detect the expression of EDAG protein in 31 cases of papillary thyroid carcinoma tissues and paracancerous tissues Data analysis EDAG knockdown lentivirus particles infected papillary thyroid cancer cell line K1, EDAG knockdown stable cell line was established to detect EDAG knockdown on cell proliferation, colony formation, cycle and apoptosis.Results showed that EDAG The protein was highly expressed in papillary thyroid carcinoma tissues, but not in the corresponding paracancerous tissues.Establishing K1 cell line stably knocked down EDAG reached about 96% knockdown effect, knocked down the cell proliferation after EDAG And the doubling time was changed from 18.49 ± 0.19 h to 19.47 ± 0.11 h, and the clonogenic capacity decreased, the proportion of G0 / G1 phase increased, and the apoptosis increased in serum-free culture.In this paper, EDAG was reported in patients with papillary thyroid carcinoma Expression and knockdown of endogenous EDAG in thyroid cancer cell line K1 inhibited cell proliferation and decreased cell clone formation, increased G0 / G1 phase and increased apoptosis, suggesting that abnormally high EDAG expression may be involved in the development of thyroid carcinoma It plays an important role.