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. 2008 Nov 21;27(1):72. doi: 10.1186/1756-9966-27-72

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Copyright © 2008 Qun et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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shows that HepG2 cells without treatment (U), and were infected with LV-siMAT2A(2A), ALV-siMAT2β (2β)and LV-siMAT2A/2β (2A/2β), cell apoptosis was induced by LV-siMAT2A, ALV-siMAT2β and LV-siMAT2A/2β, as showed in the picture "AP" stands for apoptotic peak, There was most cells into apoptosis after cells were deal with LV-siMAT2A/2β, and G1/S arrest was discovered. It was demonstrated in the Fig. 3 that cell apoptosis caused by LV-siMAT2A/2β was increased in human hepatocelluar cancer cells HepG2 compared to that induced by LV-siMAT2A, ALV-siMAT2β (P < 0.01) and control, but they all had no difference between LV-siMAT2A and LV-siMAT2β.