Pravastatin inhibits cell proliferation and increased MAT1A expression in hepatocarcinoma cells and in vivo models
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Updated: May 24, 2026

A Biomimetic Model for Liver Cancer to Study Tumor-Stroma Interactions in a 3D Environment with Tunable Bio-Physical Properties
Published on: August 7, 2020
Elizabeth Hijona1, Jesús María Banales, Lander Hijona
1Department of Gastroenterology, Donostia Hospital, Instituto Biodonostia, University of the Basque Country EHU/UPV, Ciberehd, San Sebastián, Spain. Eli.hijonamuruamendiaraz@osakidetza.net.
Background:
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.
Method:
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.
Results:
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).
Conclusion:
The combination of pravastatin + sorafenib were more effective than Sorafenib alone.
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