Loss of the Nucleosome-Binding Protein HMGN1 Affects the Rate of N-Nitrosodiethylamine-Induced Hepatocarcinogenesis in Mice

被引：12

作者：

Postnikov, Yuri V. ^{[1
]}

Furusawa, Takashi ^{[1
]}

Haines, Diana C. ^{[3
]}

Factor, Valentina M. ^{[2
]}

Bustin, Michael ^{[1
]}

机构：

[1] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA

[2] NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA

[3] NCI, Sci Applicat Int Corp, NIH, Bethesda, MD 20892 USA

来源：

MOLECULAR CANCER RESEARCH | 2014年 / 12卷 / 01期

关键词：

FATTY LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA; HEPATIC CARCINOGENESIS; DNA-REPAIR; CHROMATIN; CANCER; PHOSPHORYLATION; INFLAMMATION; EPIGENOMICS; ACTIVATION;

D O I：

10.1158/1541-7786.MCR-13-0392

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We report that HMGN1, a nucleosome-binding protein that affects chromatin structure and function, affects the growth of N-nitrosodiethylamine (DEN)-induced liver tumors. Following a single DENinjection at 2 weeks of age, Hmgn1(tm1/tm1) mice, lacking the nucleosome-binding domain of HMGN1, had earlier signs of liver tumorigenesis than their Hmgn1(+/+) littermates. Detailed gene expression profiling revealed significant differences between DEN-injected and control saline-injected mice, but only minor differences between the injected Hmgn1(tm1/tm1) mice and their Hmgn1(+/+) littermates. Pathway analysis revealed that the most significant process affected by loss of HMGN1 involves the lipid/sterol metabolic pathway. Our study indicates that in mice, loss of HMGN1 leads to transcription changes that accelerate the progression of DEN-induced hepatocarcinogenesis, without affecting the type of tumors or the final total tumor burden of these mice.

引用

页码：82 / 90

页数：9