June 25, 2024

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Aspirin’s Molecular Mechanism in Inhibiting Colorectal Cancer

Latest Research Reveals Aspirin’s Molecular Mechanism in Inhibiting Colorectal Cancer



Latest Research Reveals Aspirin’s Molecular Mechanism in Inhibiting Colorectal Cancer

Aspirin, also known as acetylsalicylic acid, has been in clinical use for over a century since its introduction in 1898, making it one of the three classic drugs in medical history. Initially used as a pain reliever, aspirin was later discovered to be a blood thinner that could help prevent heart attacks through anticoagulation. In recent years, aspirin has been found to be effective in various diseases and even plays a role in the prevention and treatment of major diseases like neurodegenerative disorders and cancer.

Colorectal cancer is the third most common cancer globally, with approximately 1.9 million new cases and 900,000 deaths reported each year. Aspirin has been identified as one of the most promising candidates for preventing colorectal cancer.

Previous studies have indicated that patients with cardiovascular diseases who take low-dose aspirin over a few years can reduce their risk of developing colorectal cancer. Furthermore, aspirin can inhibit the progression of colorectal cancer, although the underlying molecular mechanisms were not fully understood.

Latest Research Reveals Aspirin's Molecular Mechanism in Inhibiting Colorectal Cancer

Recently, researchers from the University of Munich in Germany published a research paper titled “Salicylate induces AMPK and inhibits c-MYC to activate an NRF2/ARE/miR-34a/b/c cascade resulting in the suppression of colorectal cancer metastasis” in the journal Cell Death & Disease.

This study found that aspirin and its active metabolite, salicylate, induce AMPK while inhibiting c-MYC, leading to the activation of the NRF2/ARE/miR-34a/b/c cascade, resulting in the suppression of colorectal cancer. This mechanism operates independently of the p53 signaling pathway.

The research suggests that aspirin and its derivatives may exert therapeutic effects by activating miR-34a and miR-34b/c in tumors with mutated or inactive p53.

Specifically, aspirin activates AMPK, which in turn activates the transcription factor NRF2. NRF2 directly induces the expression of miR-34a/b/c through ARE sequences. Additionally, aspirin inhibits c-MYC by activating AMPK, and c-MYC is a known inhibitor of NRF2-mediated transcriptional activation. The inhibition of c-MYC by aspirin is a necessary condition for the activation of miR-34a/b/c by NRF2. Deactivation of miR-34a/b/c largely eliminates aspirin’s inhibitory effects on the migration, invasion, and metastasis of colorectal cancer cells.

Latest Research Reveals Aspirin's Molecular Mechanism in Inhibiting Colorectal Cancer

Professor Heiko Hermeking, the corresponding author of the paper, stated that this research indicates that aspirin’s activation of miR-34 is independent of the p53 signaling pathway. This is crucial because p53 gene inactivation is the most common tumor suppressor gene in colorectal cancer. Furthermore, in most other types of cancer, p53 is often inactivated by gene mutations or viral infections. Therefore, aspirin may be used in the future for treating such cases.

Research Paper Link

Latest Research Reveals Aspirin’s Molecular Mechanism in Inhibiting Colorectal Cancer

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