Alteration of N-glycome in diethylnitrosamine-induced hepatocellular carcinoma mice: a non-invasive monitoring tool for liver cancer
Version of Record online: 26 MAY 2010
© 2010 John Wiley & Sons A/S
Volume 30, Issue 8, pages 1221–1228, September 2010
How to Cite
Liu, X.-e., Dewaele, S., Vanhooren, V., Fan, Y.-D., Wang, L., Van Huysse, J., Zhuang, H., Contreras, R., Libert, C. and Chen, C. C. (2010), Alteration of N-glycome in diethylnitrosamine-induced hepatocellular carcinoma mice: a non-invasive monitoring tool for liver cancer. Liver International, 30: 1221–1228. doi: 10.1111/j.1478-3231.2010.02279.x
- Issue online: 3 AUG 2010
- Version of Record online: 26 MAY 2010
- Received 23 February 2010Accepted 26 April 2010
- hepatocellular carcinoma (HCC);
Background and aims: There is a demand for serum markers that can routinely assess the progression of liver cancer. DENA (diethylnitrosamine), a hepatocarcinogen, is commonly used in an experimental mouse model to induce liver cancer that closely mimics a subclass of human hepatocellular carcinoma (HCC). However, blood monitoring of the progression of HCC in mouse model has not yet been achieved. In this report, we studied glycomics during the development of mouse HCC induced by DENA.
Methods: Mouse HCC was induced by DENA. Serum N-glycans were profiled using the sequencer assisted–Fluorophore-assisted carbohydrate electrophoresis technique developed in our laboratory. Possible alteration in the transcription of genes relevant to the synthesis of the changed glycans was analysed by real-time polymerase chain reaction.
Results: In comparison with the control mice that received the same volume of saline, a tri-antennary glycan (peak 8) and a biantennary glycan (peak 4) in serum total glycans of DENA mice increased gradually but significantly during progression of liver cancer, whereas a core-fucosylated biantennary glycan (peak 6) decreased. Expression of α-1,6-fucosyltransferase 8 (Fut8), which is responsible for core fucosylation, decreased in the liver of DENA mice compared with that of age-matched control mice. Likewise, the expression level of Mgat4a, which is responsible for tri-antennary, significantly increased in the liver of DENA mice (P<0.001).
Conclusions: The changes of N-glycan levels in the serum could be used as a biomarker to monitor the progress of HCC and to follow up the treatment of liver tumours in this DENA mouse model.