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The authors declare that they have no competing interests.
EH, LH and LB have designed the project. In vitro determination have been performed by JMB, JFM, MH and EH. In vivo determination have been performed by LH, PA, JA, LH and EH. Histology study have been performed by LH, JMB, PA and LH. Statistical study have been performed by LH, LB and EH. All authors write the manuscript. All authors read and approved the final manuscript.
In addition, this work was supported by grants from the Department of Health of the Basque Government 2009/111003.
Statins may have therapeutic effects on hepatocarcinoma (HCC). This type of disorder is the most common malignant primary tumour in the liver. Our objective was to determine whether pravastatin had a therapeutic effect in vitro and in vivo models.
We design in vitro and in vivo model. In vitro we used PLC and determine cell proliferation. In vivo, we used and animal model to determined, PCNA and MAT1A expression and transaminases levels.
We found that pravastatin decreases cell proliferation in vitro (cell proliferation in pravastatin group was 82%, in sorafenib group 51% and in combined group 40%) and in vivo (in pravastatin group 80%, in sorafenib group 76.4% and in combined group 72.72%). The MAT1A levels, was significantly higher in Pravastatin group (D 62%, P 94%, S 71%, P + S 91%). The transaminases levels, decreased significantly in Pravastatin group (GOT and GPT levels D 619.5 U/L; 271 U/L) (P 117.5 U/L; 43.5 U/L) (S 147 U/L; 59 U/L) (P + S 142 U/L; 59 U/L).
The combination of pravastatin + sorafenib were more effective than Sorafenib alone.