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| 敲低EDAG抑制乳头状甲状腺癌细胞的增殖 | |
| 引用本文： | 毕俊杰),董小明),郑巍薇),詹轶群),葛志强),杨晓明),李长燕). 敲低EDAG抑制乳头状甲状腺癌细胞的增殖[J]. 中国生物化学与分子生物学报, 2014, 30(6): 571-578 |
| 作者姓名： | 毕俊杰) 董小明) 郑巍薇) 詹轶群) 葛志强) 杨晓明) 李长燕) |
| 作者单位： | 1)天津大学制药工程系,天津300072；2)军事医学科学院放射与辐射医学研究所,北京100850 |
| 基金项目： | 国家优秀青年科学基金项目(No.81222005), 国家高技术研究发展计划(863计划, No.2012AA020206) |
| 摘 要： | 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. |
| 关 键 词： | 红系分化相关基因 乳头状甲状腺癌 K1 细胞增殖 |
| 收稿时间： | 2013-12-25 |
EDAG-Knockdown Inhibits Proliferation of Papillary Thyroid Carcinoma Cell |
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| BI Jun-Jie),DONG Xiao-Ming),ZHENG Wei-Wei),ZHAN Yi-Qun),GE Zhi-Qiang),YANG Xiao-Ming),LI Chang-Yan). EDAG-Knockdown Inhibits Proliferation of Papillary Thyroid Carcinoma Cell[J]. Chinese Journal of Biochemistry and Molecular Biology, 2014, 30(6): 571-578 | |
| Authors: | BI Jun-Jie) DONG Xiao-Ming) ZHENG Wei-Wei) ZHAN Yi-Qun) GE Zhi-Qiang) YANG Xiao-Ming) LI Chang-Yan) |
| Affiliation: | 1) Department of Pharmaceutical Engineering, Tianjin University, Tianjin300072,China; 2) Institute of Radiation Medicine, Academy of Military Medical Sciences, Beijing100850, China |
| Abstract: | Thyroid carcinoma is a most common endocrine malignancy tumor. The incidence in both male and female is increasing in recent years. Papillary thyroid carcinoma is the most common types in clinics. Such tumors exert better prognosis and show no pain, but has the potential to metastasize. EDAG (erythroid differentiation associated gene) is a nucleoprotein encoded by HEMGN containing 484 amino acids and expressed in hematopoietic precursor cells. EDAG was expressed in lymphoma, thyroid cancer and leukemia cells by dot blots. To study the role of EDAG in papillary thyroid carcinoma, immunohistochemistry was performed in 31 cases of papillary thyroid carcinoma with tumor and adjacent normal tissue sections. EDAG RNA interfering lentivirus was generated and infected into K1 papillary thyroid carcinoma cells for establishing a stable line. Cell proliferation, colony forming ability, cell cycle and apoptosis were analyzed in EDAG knockdown K1 cells. EDAG was highly expressed in the cytoplasm and nucleus of papillary thyroid carcinoma sections, whereas the adjacent tissues showed very low or undetectable expression. Cell proliferation was decreased as shown by the increased doubling time from 18.49±0.19 to 19.47±0.11 hours. The colony forming ability was significantly decreased with EDAG knockdown; both the G0/G1 phase and apoptosis fraction were increased. Our finding of high expression of EDAG in papillary thyroid carcinoma and EDAG knockdown to suppress cell proliferation and colony formation correlated with.the increase of G0/G1 phase and apoptosis. |
| Keywords: | erythroid differentiation associated gene（EDAG） papillary thyroid carcinoma K1 cell proliferation |
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