Elevation of protooncogene messenger RNAs in estrogen-induced kidney tumors in the hamster.
Elevation of protooncogene messenger RNAs in estrogen-induced kidney tumors in the hamster.
复制标题
雌激素诱导的仓鼠肾肿瘤中原癌基因信使 RNA 的升高。
DOI:
10.1093/carcin/13.4.601
复制
发表时间:
1992
期刊:
影响因子:
4.7
通讯作者:
Stancel,GM
中科院分区:
文献类型:
--
作者:
Liehr,JG;Chiappetta,C;Roy,D;Stancel,GM
Cellular oncogenes such as c-fos, c-junand c-mycare expressed prior to estrogen-induced growth of normal target tissues such as rodent uterus. Transient increases in the levels of these genes are induced by the administration of estradiol and are followed by DNA replication. In this study, we examined the expression of these three oncogenes in estradiolinduced kidney tumors in Syrian hamsters in order to understand mechanistic aspects of hormonal carcinogenesis. Kidney tumors were induced in all male Syrian hamsters treated chronically with estradiol for 7 or 9 months, whereas neoplasms were not detected in animals treated for 5 months. mRNA levels offos,mycandjunwere elevated 15-, 4- and 6-fold respectively in kidney tumors of estradiol-treated hamsters (9 months) compared with age-matched untreated control kidneys. The expression of all three protooncogenes was also increased in the kidney tissue surrounding tumors, though there was no consistent pattern in the ratios of transcripts in the tumor and kidney tissues. After 7 months of estrogen treatment, kidney tumors also contained elevated amounts of c-fos, c-junand c-myctranscripts at levels comparable with older tumors. In abdominal metastases of hamster kidney tumors, mRNA levels offos,mycandjunwere elevated 9-, 12- and 3-fold respectively over control levels. In kidneys of hamsters treated with estradiol for 5 months, in which tumors were not yet detected, the expression of protooncogenes was slightly increased. Ratios of c-fos, c-mycand c-junin estrogen-treated (5 months) over control tissue were 1.4, 1.1and 1.3 respectively. Overexpression of cellular oncogenes such as c-fos, c-junand c-mycmay have played a role in the induction and growth of kidney tumors by estradiol in hamsters.