Colorectal cancer, also known as bowel cancer, is a global health concern with millions of new cases and deaths reported annually.
Among the substances explored for its prevention, aspirin, or acetylsalicylic acid, has shown significant promise.
Studies have indicated that regular low-dose aspirin intake can reduce the risk of colorectal cancer, especially in patients with cardiovascular diseases.
Additionally, aspirin has demonstrated the ability to inhibit the progression of colorectal cancer.
In a breakthrough discovery, a team led by Professor Heiko Hermeking at LMU Munich has unraveled the molecular mechanisms through which aspirin exerts its inhibitory effects on colorectal cancer.
Background: The Promise of Aspirin
The link between aspirin and colorectal cancer prevention has long intrigued researchers.
Previous investigations found that long-term aspirin use in cardiovascular patients correlated with a decreased risk of developing colorectal cancer.
However, the intricate molecular processes underlying this phenomenon remained a mystery.
Research Evidence: Aspirin’s Molecular Actions
In a study published in the journal Cell Death and Disease, the LMU Munich researchers have uncovered the molecular pathways through which aspirin inhibits colorectal cancer. The key findings include:
MicroRNA Production: Aspirin triggers the production of two microRNA molecules, specifically miR-34a and miR-34b/c, which exhibit tumor-suppressive properties. These microRNAs play a vital role in colorectal cancer prevention.
AMPK Activation: Aspirin binds to and activates an enzyme called AMPK (AMP-activated protein kinase). AMPK, in turn, influences the behavior of NRF2, a transcription factor responsible for regulating gene expression.
NRF2 Activation: Activated AMPK alters NRF2 in a way that it moves into the cell nucleus. Inside the nucleus, NRF2 activates the expression of the miR-34 genes, which are crucial for the inhibitory effects of aspirin on colorectal cancer cells.
c-MYC Suppression: Aspirin also acts to suppress c-MYC, an oncogene product. c-MYC typically inhibits NRF2, but aspirin’s interference allows NRF2 to function effectively.
Implications and Future Directions
These findings are significant for several reasons:
Independence from p53 Pathway: While it was previously known that the miR-34 genes were activated by the p53 signaling pathway, this study reveals that aspirin’s activation of miR-34 occurs independently of p53.
This is particularly important because the p53 gene is frequently inactivated in colorectal cancer, as well as in many other types of cancer.
Therapeutic Potential: Aspirin’s effectiveness in activating miR-34 genes suggests its potential therapeutic use, especially in cases where the p53 tumor suppressor gene is inactive or impaired due to mutations or viral factors.
This opens doors for aspirin to be employed as a targeted treatment option in colorectal cancer and potentially other cancer types.
Conclusion
The study conducted by the LMU Munich researchers sheds light on the intricate molecular mechanisms by which aspirin inhibits colorectal cancer.
By promoting the production of tumor-suppressive microRNAs, activating AMPK, and modulating NRF2 and c-MYC, aspirin demonstrates its potential as a preventive and therapeutic agent.
These findings hold promise for future advancements in colorectal cancer management and pave the way for more targeted and effective treatments.
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The research findings can be found in Cell Death & Disease.
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