AI Article Synopsis
- A study reveals that HMGN1, a protein involved in chromatin structure, influences the growth of liver tumors caused by N-nitrosodiethylamine (DEN) in mice.
- Mice lacking HMGN1 (Hmgn1(tm1/tm1)) showed earlier signs of liver tumors compared to normal mice after DEN exposure, suggesting HMGN1 slows tumor development.
- Gene profiling indicated changes in lipid/sterol metabolism due to the loss of HMGN1, impacting how the liver tumors progress but not their type or overall quantity.
Article Abstract
Unlabelled: 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 DEN injection 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.
Implications: Loss of HMGN1 leads to accelerated progression of DEN-induced hepatocarcinogenesis in mice.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3905959 | PMC |
| http://dx.doi.org/10.1158/1541-7786.MCR-13-0392 | DOI Listing |
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