Statins, commonly used to lower cholesterol levels, have been discovered to potentially inhibit the spread of cancer. Research has shown that cancer cells can rapidly spread to other organs, making treatments less effective and reducing survival rates. However, recent studies suggest that statins, a type of cholesterol-lowering medication, could serve as an unexpected ally in combating this spread of cancer.
The primary danger in cancer progression typically lies in metastases, where cancer cells break away from the original tumor and migrate to other parts of the body, forming new tumors. A gene known as MACC1, which was identified over a decade ago by a research team led by Professor Ulrike Stein, plays a significant role in facilitating this spread of cancer cells. When cancer cells express the MACC1 gene, they become more proficient at growing, spreading, and invading new tissues. MACC1 has been associated with various types of solid tumors, such as those found in the liver, breast, and stomach.
In a surprising development, Professor Stein and Dr. Robert Preißner from Charité – Universitätsmedizin Berlin discovered that statins can effectively inhibit the expression of the MACC1 gene. While statins are commonly prescribed to lower cholesterol levels and reduce the risk of heart disease, they may also possess the ability to impede the spread of cancer. Experiments using mice genetically modified to overexpress MACC1 showed that statin treatment significantly suppressed tumor growth and cancer spread. Even at lower dosages equivalent to those used in humans, statins continued to demonstrate strong benefits.
Further research expanded to real-world patient data, analyzing health records from two medical centers. Among the almost 278,000 patients examined, those taking statins, particularly simvastatin and atorvastatin, exhibited lower rates of cancer development. Patients on statins had a reduced risk of cancer by approximately 28% and a 36% lower risk of death compared to those not taking statins.
Overall, these findings suggest that statins may hold promise in mitigating the metastasis of cancer cells and improving patient outcomes in cancer treatment.
The expression of Metastasis-associated in colon cancer 1 (MACC1) was inhibited by certain drugs in vitro, as reported by Clinical and Translational Medicine. The specific dosage did not appear to significantly impact the outcome. Patients taking either a low or high dose experienced a similar reduction in cancer risk. Notably, Atorvastatin demonstrated the most substantial effect, decreasing cancer risk by nearly 60%. Other statins including Fluvastatin, Pravastatin, and Rosuvastatin also displayed strong protective effects. Simvastatin had a lesser impact, while data on Lovastatin was limited due to lower usage.
Addressing potential confounding factors is crucial when analyzing real-world data, as various variables can influence outcomes. To address this issue, researchers conducted propensity score matching to align statin users and non-users based on characteristics like age and gender. This statistical adjustment helped ensure that observed differences in cancer rates were not influenced by unrelated factors.
Statin treatment was found to reduce tumor burden and metastasis formation in vivo. In a study involving SCID-beige mice xenografted with HCT116/CMVp-Luc cells, daily doses of Fluvastatin or Atorvastatin were administered, resulting in decreased tumor growth compared to the control group.
Even after excluding medications that could affect cancer risk, such as aspirin and furosemide, statins continued to exhibit a strong protective effect, pointing to MACC1 suppression as a likely biological mechanism. The researchers reported a significant and consistent cancer-preventive signal even after adjusting for known confounders.
Statins demonstrated preventive effects across various cancer types, including colon, liver, and secondary tumors. The protective effect was particularly pronounced in liver cancer, with a 65% reduction in risk, while colon cancer risk decreased by 56%, aligning with previous research findings.
The researchers expanded their analysis to a larger cohort using the TriNetX platform, confirming their initial results with an additional 132,072 patients. This validation supported the notion that statins have a genuine preventive effect on cancer development.
At the molecular level, statins were shown to lower MACC1 expression in colon, pancreatic, and gastric cancer cells, inhibiting their growth and spread. Simvastatin and Atorvastatin were particularly effective in reducing MACC1 levels, correlating with their ability to prevent cancer progression in patients. Reintroducing MACC1 into cells weakened the anticancer effects of statins, emphasizing the gene’s role in promoting cancer growth and the importance of blocking it.
A recent study published in Clinical and Translational Medicine found that in mice treated with statins at human-equivalent doses, tumors decreased in size and fewer metastases developed. The effectiveness of the statins was most notable in cases where MACC1 levels were initially high, indicating a potential for this gene to help identify individuals who could benefit the most from this treatment.
Looking ahead, the fact that statins are already approved and widely used provides a significant advantage over novel medications. If further research confirms their ability to inhibit cancer spread, statins could be swiftly integrated into cancer treatment protocols. However, experts caution that these findings are preliminary and more studies are needed to validate them in human patients with elevated MACC1 levels. Therefore, individuals should not take statins solely for cancer prevention without consulting a healthcare provider, as these medications may have side effects and may not be suitable for everyone.
Nevertheless, the results show promise. For individuals already taking statins for cholesterol management, there could be an additional benefit of reduced risk of developing or succumbing to cancer. The research findings can be accessed online in Clinical and Translational Medicine.
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