Establishment of an oral squamous cell carcinoma cell line (NOS-1) exhibiting amplification of the erbB-1 oncogene and point mutation of p53 tumor suppressor gene:: its biological characteristics and animal model of local invasion by orthotopic transplantation of the cell line
Establishment of an oral squamous cell carcinoma cell line (NOS-1) exhibiting amplification of the erbB-1 oncogene and point mutation of p53 tumor suppressor gene:: its biological characteristics and animal model of local invasion by orthotopic transplantation of the cell line
复制标题
DOI：
10.1016/s1368-8375(00)00088-9
复制
发表时间：
2001-06-01
期刊：
影响因子：
4.8
通讯作者：
Komori, T
中科院分区：
文献类型：
--
作者：
Ji, ZW;Oku, N;Komori, T
我们建立了一个新的癌细胞系，NOS-I，这是来自人口腔原发性鳞状细胞癌。采用遗传霉素处理，以消除污染的成纤维细胞，并在培养的早期阶段富集肿瘤细胞。光镜和电镜观察显示NOS-I细胞呈上皮样形态，免疫组化证实其来源于上皮。突变型p53蛋白的过表达，p53在密码子248处的点突变与从CGG到TGG的转换，以及erbB-1癌基因/表皮生长因子受体基因的扩增也在NOS-1细胞中观察到。当移植到裸鼠背部皮下时，NOS-1细胞在裸鼠体内形成肿瘤。此外，它们可原位移植于裸鼠舌内，舌内移植瘤呈弥漫性浸润，不形成包膜。NOS-1细胞可用于阐明p53失活和erbB-1癌基因扩增的机制，以及口腔癌的治疗。(C)2001爱思唯尔科技有限公司版权所有。
We established a new cancer cell line, NOS-I, which was derived from a human oral primary squamous cell carcinoma. Geneticin treatment was adopted to eliminate contaminating fibroblasts and to enrich tumor cells in the early stage of the culture. The NOS-I cells showed epithelial morphological features with light and electron microscopy, and immunohistochemical analysis confirmed their epithelial origin. Overexpression of mutant p53 protein, a p53 point mutation at codon 248 with transition from CGG to TGG, and amplification of the erbB-1 oncogene/epidermal growth factor receptor gene were also observed in NOS-1 cells. The NOS-1 cells formed tumors in nude mice when transplanted subcutaneously into their backs. Further, they were transplantable orthotopically in the tongues of nude mice, and the transplanted tumors in the tongue show-ed diffuse invasion without forming capsules. The NOS-1 cells were useful for elucidating the mechanism involving p53 inactivation and erbB-1 oncogene amplification, as well as treatment of oral cancer. (C) 2001 Elsevier Science Ltd. All rights reserved.