在NIH3T3细胞中高表达EDAG-1基因导致细胞恶性转化  

Overexpression of EDAG-1 in NIH3T3 Cells Leads to Malignant Transformation

作　　者：闾军[1] 许望翔[2] 汪思应[2] 江岩[2] 李长燕[2] 蔡卫民[1] 杨晓明[2] 

机构地区：[1]浙江大学医学院第一附属医院传染病研究所,杭州710006 [2]军事医学科学院放射医学研究所,北京100850

出　　处：《生物化学与生物物理学报》2002年第1期95-98,共4页

基　　金：国家自然科学基金 (No .396 70 36 6 );国家杰出青年基金 (No .30 0 2 5 0 18)资助项目~~

摘　　要：探讨一种新近克隆的特异表达在造血系统组织和细胞中的胚胎发育相关新基因 (EDAG 1)的生物学功能。构建EDAG 1真核表达载体pcDNA3.1(+) EDAG 1,以脂质体法将其稳定转染入NIH3T3细胞中 ,结果发现高表达EDAG 1的NIH3T3细胞失去了正常的平行走向及接触抑制现象 ,侵袭力较正常增强约 10倍并获得锚定不依赖生长能力。将该细胞株皮下接种裸鼠 ,受鼠在 4周左右 10 0 % (6 / 6 )成瘤。这些结果表明EDAG 1是一种具有转化活性的新基因 ,可能与肿瘤发生。To study the biological function of EDAG-1, a novel gene cloned by our lab recently, the EDAG-1 cDNA was subcloned into pcDNA3.1(+) vector and transfected into NIH3T3 cells by Lipofect AMINE methods. Overexpression of EDAG-1 in NIH3T3 cells resulted in loss of cell contact inhibition, anchorage-independent growth in soft agar and tumor formation in nude mice. These results suggest that EDAG-1 is a transforming gene and may be associated with the development of tumors, especially in hematopoietic system.

关 键 词：EDAG-1 基因表达 恶性转化 NIH3T3细胞 肿瘤发生 

分 类 号：Q786[生物学—分子生物学]