ALTERED GROWTH OF HUMAN COLON CANCER CELL-LINES DISRUPTED AT ACTIVATED KI-RAS
ALTERED GROWTH OF HUMAN COLON CANCER CELL-LINES DISRUPTED AT ACTIVATED KI-RAS
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DOI：
10.1126/science.8465203
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发表时间：
1993-04-02
期刊：
影响因子：
56.9
通讯作者：
SASAZUKI, T
中科院分区：
文献类型：
--
作者：
SHIRASAWA, S;FURUSE, M;SASAZUKI, T
激活Ki-ras原癌基因的点突变存在于约50%的人类结直肠肿瘤中。为了研究这些突变的功能意义，在两个人结肠癌细胞系DLD-1和HCT 116中激活的Ki-ras基因被同源重组破坏。与亲本细胞相比，在激活的Ki-ras基因被破坏的细胞形态改变，失去了锚定非依赖性生长的能力，在体外和裸鼠中生长更慢，并显示c-myc的表达减少。因此，活化的Ki-ras基因通过改变细胞分化和细胞生长在结直肠肿瘤发生中起关键作用。
Point mutations that activate the Ki-ras proto-oncogene are present in about 50 percent of human colorectal tumors. To study the functional significance of these mutations, the activated Ki-ras genes in two human colon carcinoma cell lines, DLD-1 and HCT 116, were disrupted by homologous recombination. Compared with parental cells, cells disrupted at the activated Ki-ras gene were morphologically altered, lost the capacity for anchorage-independent growth, grew more slowly both in vitro and in nude mice, and showed reduced expression of c-myc. Thus, the activated Ki-ras gene plays a key role in colorectal tumorigenesis through altered cell differentiation and cell growth.