Aspirin activates protective genes against bowel cancer

Salicylate suppresses colorectal cancer metastasis via AMPK activation.

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The new study from Luddwig Maximilians Universitat Munchen focuses on a significant finding in bowel cancer research. It underscores the potential of aspirin to activate specific protective genes that play a vital role in preventing or inhibiting the development and progression of bowel cancer, also known as colorectal cancer.

Colorectal cancer, also known as bowel cancer, ranks as the third most common cancer worldwide, causing approximately 1.9 million new cases and 900,000 deaths each year. Preventive solutions are urgently needed. Aspirin, or acetylsalicylic acid, has emerged as a promising candidate for colorectal cancer prevention. 

Research has revealed that taking low doses of aspirin over several years can reduce the risk of colorectal cancer, especially in patients with heart conditions. Moreover, aspirin can slow down the progression of colorectal cancer. A team led by Professor Heiko Hermeking at LMU explored the specific molecular mechanisms behind these effects.

In a study published in the journal Cell Death and Disease, researchers found that aspirin triggers the production of two cancer-fighting microRNA molecules, miR-34a and miR-34b/c. Aspirin achieves this by binding to and activating the enzyme AMPK, which, in turn, changes the behavior of NRF2. This protein moves into the cell nucleus and turns on the miR-34 genes. As part of this process, aspirin also suppresses c-MYC, a gene that typically blocks NRF2 from working.

The findings underscore the essential role of miR-34 genes in mediating aspirin’s capacity to hinder colorectal cancer cells. Without miR-34, aspirin loses its ability to impede the movement, invasion, and spread of cancer cells. It’s important to note that the transcription factor p53 is responsible for triggering miR-34 genes and facilitating their influence.

Hermeking said, “Our results show, however, that activation of the miR-34 genes by aspirin takes place independently of the p53 signaling pathway. “This is important because the p53-encoding gene is the most commonly inactivated tumor suppressor gene in colorectal cancer. In most other kinds of cancer, moreover, p53 is inactivated by mutations or viruses in the majority of cases. Aspirin could, therefore, be employed therapeutically in such cases in the future.”

In conclusion, the study “Bowel Cancer: Aspirin Activates Protective Genes” highlights the potential benefits of aspirin in activating specific protective genes associated with colorectal cancer. This finding could have a significant impact on how we approach the prevention and treatment of bowel cancer, potentially leading to more accessible and effective strategies for reducing the burden of this disease.

Journal reference:

  1. Liu, C., Rokavec, M., Huang, Z. et al. Salicylate induces AMPK and inhibits c-MYC to activate a NRF2/ARE/miR-34a/b/c cascade, resulting in suppression of colorectal cancer metastasis. Cell Death Disease. DOI: 10.1038/s41419-023-06226-9.

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