German scientists have identified a signaling pathway by which this drug can inhibit colon or rectal cancer.
- Through a system, led by an enzyme called AMPK, aspirin helps activate a protective cleaning system in our cells.
- Additionally, this medication affects molecules, called miR-34a/b/c, which can tell a cell to repair itself, stop dividing, or die.
- A particular variation in the miR-34 genes affects how aspirin can work.
It is the third most common cancer in men and the second in women. Colorectal cancer develops from the cells that line the inner lining of the colon (in about 40% of cases) or rectum (60%). In a recent study, researchers from the Louis-Maximilien University in Munich (Germany) revealed that taking aspirin could reduce the risk of suffering from this large intestine cancer.
Low doses of aspirin may reduce the risk of colorectal cancer
To reach this conclusion, they carried out work published in the journal Cell Death & Disease. As part of their study, the scientists looked at the underlying molecular mechanisms of aspirin that prevent or slow the progression of colon or rectal cancer. The results showed that when patients with cardiovascular disease took low doses of the drug for several years, it reduced their risk of colorectal cancer. Additionally, aspirin may inhibit the progression of colorectal cancer.
In detail, aspirin induces the production of two tumor-suppressive microRNA (miRNA) molecules, called “miR-34a” and “miR-34b/c”. For this, acetylsalicylic acid binds to and activates the enzyme AMPK, which in turn modifies the transcription factor NRF2 such that it migrates into the cell nucleus and activates the expression of miR-34 genes. . For this activation to occur, aspirin suppresses the oncogene product c-MYC, which otherwise inhibits NRF2.
Colorectal cancer: the role of miR-34 genes in the inhibitory effect of aspirin on cells
According to the authors, miR-34 genes are required to mediate the inhibitory effect of aspirin on colorectal cancer cells. Aspirin was thus unable to prevent migration, invasion and metastasis in miR-34-deficient cancer cells. It was already known that miR-34 genes are induced by the transcription factor p53 and mediate its effects.
“Our results, however, show that activation of miR-34 genes by aspirin occurs independently of the p53 signaling pathway. This is important because the gene encoding p53 is the most commonly inactivated tumor suppressor gene in cancer colorectal. Additionally, in most other types of cancer, p53 is inactivated by mutations or viruses in the majority of cases. So aspirin could be used therapeutically in such cases in the future.” explained Heiko Hermeking, author of the research, in a statement.