Expression of the c-myc, c-fos and c-rasHa protooncogenes during sex-differentiated rat liver carcinogenesis in the resistant hepatocyte model.
Expression of the c-myc, c-fos and c-rasHa protooncogenes during sex-differentiated rat liver carcinogenesis in the resistant hepatocyte model.
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耐药肝细胞模型中性别分化大鼠肝癌发生过程中c-myc、c-fos和c-rasHa原癌基因的表达。
DOI：
10.1093/carcin/10.10.1793
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发表时间：
1989
期刊：
影响因子：
4.7
通讯作者：
Gustafsson,JA
中科院分区：
文献类型：
--
作者：
Porsch-Hällström,I;Blanck,A;Eriksson,LC;Gustafsson,JA
已在根据耐药肝细胞模型治疗的大鼠中研究了原癌基因c-myc、c-los和c-rasHa的表达。在选择阶段，研究了雄性和雌性大鼠肝脏中原癌基因的表达，此时雄性中推定的癌前病灶/结节的生长明显更快，并与雄性晚期结节和肝细胞癌中的表达进行了比较。在部分肝切除术后的前 16 小时内，在接受选择/促进方案但不接受二乙基亚硝胺的起始动物和“对照”动物中，c-losand c-myc 的表达在两性中均显示出短暂的 2 至 3 倍增加，分别在 0.5 小时和 2-4 小时达到最大值。所有组中的 c-rasHa 在 16-24 小时均表现出适度增加（1.5 倍）。 c-myc表达的第二次增加（2倍）在部分肝切除术后24小时开始，并在已启动的雄性中持续整个选择期，而在雌性和未启动的雄性中则没有变化。在开始的男性部分肝切除术后 24 小时，c-fos 表达也显示出短暂的增加。在癌前结节和肝细胞癌中，c-mycan和c-los的表达增加了2至4倍，而c-rasHa表达没有变化。总之，在癌前病变的早期生长过程中，观察到 c-mycan 和 c-los 表达的性别差异，可能反映了这些基因的表达与耐药肝细胞模型中对促进的性别差异反应之间的联系。此外，在肝癌晚期阶段的过度表达可能表明所讨论的原癌基因的表达与该模型中多步致癌的整个过程有关。
The expression of the protooncogenes c-myc, c-losand c-rasHahas been studied in rats treated according to the resistant hepatocyte model. Protooncogene expression was studied in male and female rat liver during the selection phase, when the outgrowth of putative preneoplastic foci/nodules is markedly faster in males, and compared with the expression in advanced nodules and hepatocellular carcinomas in males. During the first 16 h after partial hepatectomy the expression of c-losand c-mycshowed transient, 2- to 3-fold, increases in both sexes, both in initiated and in ‘control’ animals, receiving the selection/promotion regimen but no diethyl nitrosamine, with a maximum at 0.5 and 2–4 h respectively. c-rasHaexhibited a moderate increase (1.5-fold) at 16–24 h in all groups. A second increase in c-mycexpression (2-fold) started 24 h after partial hepatectomy and lasted over the entire selection period in initiated males, while it was unchanged in females and uninitiated males. The c-fosexpression also showed a short-lived increase 24 h post partial hepatectomy in initiated males. The expression of c-mycand c-loswas increased 2- to 4-fold in both preneoplastic nodules and hepatocellular carcinomas, whereas c-rasHaexpression was unchanged. In conclusion, sex differences were observed in the expression of c-mycand c-losduring the early outgrowth of preneoplastic lesions, possibly reflecting a connection between the expression of these genes and the sex differentiated response to promotion in the resistant hepatocyte model. Furthermore, an overexpression also in later stages of liver carcinogenesls might indicate that expression of the protooncogenes in question is related to the entire process of multistep carcinogenesis in this model.
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