Abstract
The importance of statins in cancer has been discussed in many studies. They are known for their anticancer properties against solid tumors of the liver or lung, as well as diffuse cancers, such as multiple myeloma or leukemia. Currently, the most commonly used statins are simvastatin, rosuvastatin and atorvastatin. The anti-tumor activity of statins is largely related to their ability to induce apoptosis by targeting cancer cells with high selectivity. Statins are also involved in the regulation of the histone acetylation level, the disturbance of which can lead to abnormal activity of genes involved in the regulation of proliferation, differentiation and apoptosis. As a result, tumor growth and its invasion may be promoted, which is associated with a poor prognosis. High levels of histone deacetylases are observed in many cancers; therefore, one of the therapeutic strategies is to use their inhibitors. Combining statins with histone deacetylase inhibitors can induce a synergistic anticancer effect.
Highlights
The aim of this paper is to present the current state of knowledge on the potential mechanisms of statin action in reducing the risk of cancer and its therapy
Simvastatin tested in a mouse model in which a human lung cancer xenograft was introduced inhibited tumor growth and bone metastasis, which occurred with a simultaneous reduction in MAPK/ERK activity [57]
The results of the 2019 metaanalysis, which examined data collected from meta-analyzes of randomized controlled trials (RCTs) and observational studies assessing the effect of statins on the risk of cancer, should be taken into account
Summary
3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, known as statins, are a commonly used and well-tolerated class of drugs used in lipid disorders, especially in cases of hypercholesterolemia. Another study proved that simvastatin deregulated mutant p53 protein, activating the caspase-dependent apoptotic pathway and reducing the mobility of p53-mutated lung cancer cells [23] In addition to their angiostatic effect, statins inhibit the synthesis of cytokines, including interleukin (IL-) IL-1β, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α). One of the key mechanisms of the antitumor activity of statins is the angiostatin effect in neoplastic lesions [64,65] It is based on the expression modulation of anti- and pro-angiogenic factors, including VEGF, FGF and IGF-1, leading to the inhibition of angiogenesis and, as a result, reduction in metastatic capacity of cancer cells [64,66,67]. The great potential of statins in terms of their use as drugs delaying progression and expansion of cancer has been proven in the course of experimental work [20,51,70]
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