N-亚硝基双（2-氧代丙基）胺诱导的仓鼠胰腺导管腺癌及其细胞系中中期因子的过表达。
Overexpression of midkine in pancreatic duct adenocarcinomas induced by N-Nitrosobis(2-oxopropyl)amine in hamsters and their cell lines.
作者信息
Tsutsumi M, Kadomatsu K, Tsujiuchi T, Sakitani H, Ikematsu S, Kubozoe T, Yoshimoto M, Muramatsu T, Sakuma S, Konishi Y
机构信息
Department of Oncological Pathology, Cancer Center, Nara Medical University, Kashihara, Nara 634-8521, Japan.
出版信息
Jpn J Cancer Res. 2000 Oct;91(10):979-86. doi: 10.1111/j.1349-7006.2000.tb00874.x.
The expression of midkine (MK) was investigated in pancreatic ductal hyperplasias, atypical hyperplasias and adenocarcinomas induced by N-nitrosobis(2-oxopropyl)amine (BOP) in hamsters, and in hamster ductal adenocarcinoma cell lines (HPD-1NR, -2NR and -3NR). MK mRNA was clearly overexpressed in invasive pancreatic duct adenocarcinomas (PCs) and the three cell lines as assessed by northern blot analysis, and MK protein expression increased from ductal hyperplasia through atypical hyperplasias, intraductal carcinomas and invasive PCs by immunohistochemistry. The extent of overexpression of MK mRNA in PCs was almost the same as in hamster whole embryonic tissue. MK is reported to be a retinoid-responsive gene, but MK mRNA expression was not affected by treatment with all-trans retinoic acid (tRA) or N-(4-hydroxyphenyl)retinamide (4-HPR) in HPD-1NR cells. The results thus suggest that MK expression is involved in the development and progression of pancreatic ductal adenocarcinomas induced by BOP in hamsters, with loss of upregulation by retinoic acid.
研究了仓鼠中由N-亚硝基双（2-氧代丙基）胺（BOP）诱导的胰腺导管增生、非典型增生和腺癌以及仓鼠导管腺癌细胞系（HPD-1NR、-2NR和-3NR）中中期因子（MK）的表达。通过Northern印迹分析评估，MK mRNA在浸润性胰腺导管腺癌（PCs）和这三种细胞系中明显过表达，并且通过免疫组织化学检测，MK蛋白表达从导管增生经非典型增生、导管内癌到浸润性PCs逐渐增加。PCs中MK mRNA的过表达程度与仓鼠全胚胎组织中的几乎相同。据报道MK是一种视黄酸反应性基因，但在HPD-1NR细胞中，MK mRNA表达不受全反式维甲酸（tRA）或N-（4-羟基苯基）视黄酰胺（4-HPR）处理的影响。因此，结果表明MK表达参与了仓鼠中由BOP诱导的胰腺导管腺癌的发生和发展，且视黄酸上调作用缺失。
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