4.3 Review

Prevention of Hepatocellular Carcinoma by Statins: Clinical Evidence and Plausible Mechanisms

Journal

SEMINARS IN LIVER DISEASE
Volume 39, Issue 2, Pages 141-152

Publisher

THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0039-1679956

Keywords

statin; hepatocellular carcinoma; risk; prevention; pathogenesis

Funding

  1. Bio & Medical Technology Development Program of the NRF, Korea, MSIP [2016R1A2B4013029]
  2. National Research Foundation of Korea [2016R1A2B4013029] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Statins, or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, are widely used to treat hypercholesterolemia for primary and secondary prevention of cardiovascular disease. Statins inhibit HMG-CoA reductase, the rate-limiting step in cholesterol synthesis, and modulate the downstream signaling of the mevalonate pathway. In addition to the primary effect, the antitumor effect of statins can be associated with mevalonate pathway-mediated and nonmevalonate pathway-mediated mechanisms, which improve endothelial function and lead to proapoptotic, antiproliferative, antiinflammatory, and antifibrotic properties. Statins are implicated in the improvement of metabolic status. Statins are orally available and safely and widely used for long-term treatment; they represent a novel approach for the prevention and treatment for hepatocellular carcinoma (HCC). Although several observational studies and experimental studies have revealed the preventive and therapeutic potential of statins for HCC treatment, further prospective interventional studies and randomized control trials are warranted to confirm these observations.

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