Correlation between Ha-ras gene amplification and spontaneous metastasis in NIH 3T3 cells transfected with genomic DNA from human skin cancers.

Correlation between Ha-ras gene amplification and spontaneous metastasis in NIH 3T3 cells transfected with genomic DNA from human skin cancers.
复制标题

转染人类皮肤癌基因组 DNA 的 NIH 3T3 细胞中 Ha-ras 基因扩增与自发转移之间的相关性。

DOI:
10.1007/bf01753682
复制
发表时间:
1989
影响因子:
4
通讯作者:
Bales,ES
Bales,ES
中科院分区:
医学3区
文献类型:
--
作者:
Ananthaswamy,HN;Price,JE;Tainsky,MA;Goldberg,LH;Bales,ES

文献摘要

相似文献

我们以前的研究表明,一些人皮肤癌的DNA通过DNA介导的基因转移进入NIH3T3细胞后,含有激活的ha-rasono基因,能够诱导肿瘤转化。此外,我们还发现,将人皮肤癌DNA导入NIH3T3细胞,不仅能诱导S.C.注射部位的肿瘤也会自发转移到100%注射的裸鼠的肺部。在本研究中,我们研究了Ha-raso基因扩增与不同人皮肤癌DNA转染体诱导的肿瘤转移潜能之间的关系。从裸鼠肿瘤细胞系中提取细胞总RNA,通过Northern印迹杂交分析~(32)P标记的缺口翻译的Ha-ras探针。裸鼠肿瘤细胞系通过静脉注射后形成肺集落的能力来评估其转移潜能。或者南加州大学。注射。研究发现,只有高水平表达Ha-ras基因转录本的肿瘤才能诱发自发性转移。注射。Ha-raso基因扩增水平与实验性转移的相关性不明显。这些结果表明,Ha-raso基因的扩增和过表达可能在细胞逃离原发肿瘤的过程中起作用,而不是在细胞在循环系统中存活和在次生部位定植的能力中起作用。
Our previous studies have shown that DNA from some human skin cancers contained activated Ha-rasoncogenes capable of inducing tumorigenic transformation when introduced into NIH 3T3 cells by DNA-mediated gene transfer. In addition, we found that NIH 3T3 cells transfected with DNA from one of the human skin cancers not only induced s.c. tumors at the site of injection but also metastasized spontaneously to the lungs in 100 per cent of nude mice injected. In this present study we examined the relationship between Ha-rasoncogene amplification and metastatic potential in tumors induced by various human skin cancer DNA-transfectants. Total cellular RNA was extracted from nude mouse tumor cell lines and analyzed by northern blot hybridization to a32P-labeled, nick-translated Ha-rasprobe. The metastatic potential of nude mouse tumor cell lines was assessed by their ability to form lung colonies after i.v. or s.c. injection. It was found that only the tumors expressing high levels of Ha-rasgene transcripts induced spontaneous metastasis after s.c. injection. There appeared to be little correlation between the level of Ha-rasoncogene amplification and experimental metastasis. These results suggest that amplification and overexpression of Ha-rasoncogene may play a role in the escape of cells from the primary tumor rather than in the ability of cells to survive in the circulatory system and colonize secondary sites.