Antitumoral and cardioprotective roles of statins: underlying types, mechanisms, current evidence, and emerging perspectives

Statins are widely recognized as cholesterol-lowering agents that reduce the risk of myocardial infarction and stroke, but emerging evidence highlights their broader therapeutic potential, particularly in oncology. By inhibiting the mevalonate pathway, statins disrupt the activation of small GTP-binding proteins such as Ras and Rho, key mediators of cancer cell proliferation, migration, and survival. This disruption triggers multiple antitumoral mechanisms, including cell cycle arrest, induction of apoptosis, suppression of angiogenesis, and inhibition of metastatic progression. Preclinical studies across diverse tumor models-most notably breast cancer-demonstrate robust anticancer activity. Clinical data now echo these findings, with observations suggesting that patients on statins, particularly hydrophilic agents like rosuvastatin, may achieve improved disease- free survival and reduced recurrence rates. Importantly, statins also confer cardioprotective effects, mitigating chemotherapy-induced cardiotoxicity through their antioxidant and anti-inflammatory properties-an advantage of significant relevance in long-term survivorship. Despite this promising dual benefit, statins have not yet been integrated into standard oncology practice. Rigorous clinical trials are required to define the patient subgroups most likely to benefit, optimize combination strategies, and establish safety in the oncologic setting. If validated, statins could represent a cost-effective, widely accessible adjunct to improve cancer outcomes while preserving cardiovascular health.