Antidiabetic drug's potential in cancer control

Researchers at Flinders University have explored the potential of using an antidiabetic drug to manage tumor growth, with promising implications for developing enhanced cancer treatments. This study focused on metformin, a medication commonly prescribed for type 2 diabetes, and its effects on colorectal cancer cells. The researchers' findings suggest that metformin can be leveraged to create new therapies aimed at combating cancer more effectively.

Past epidemiological research has indicated that metformin provides some protection against certain cancers, including colorectal cancer, for those with diabetes. The team at Flinders University aimed to delve deeper into the mechanisms behind this protective effect. They sought to determine how metformin affects cancer cell behavior and how these effects could inform future cancer treatments.

Dr. Ayla Orang, the lead author from Flinders University's College of Medicine and Public Health, explained that the study utilized advanced techniques to examine how metformin inhibits the growth and multiplication of colorectal cancer cells. The drug achieves this by regulating specific cellular pathways responsible for growth and division. The critical discovery was that metformin increases the levels of specific microRNAs, small RNA molecules that can turn off genes involved in cell growth and division. This action acts as a circuit breaker, halting the uncontrolled proliferation of cancer cells.

Specifically, the study highlighted the role of microRNAs such as miR-2110 and miR-132-3p, which target genes that drive tumor growth. By increasing these microRNAs, metformin effectively slows down the progression of cancer. The researchers propose that these findings could lead to the development of RNA-based therapies that target these microRNAs to treat cancer.

The study, titled "Restricting Colorectal Cancer Cell Metabolism with Metformin: An Integrated Transcriptomics Study," employed cutting-edge techniques to analyze the complete set of genes expressed in colon cancer cells. This comprehensive approach helped the team understand how metformin influences the cells at a molecular level. They discovered that metformin boosts the levels of microRNAs miR-2110 and miR-132-3p, which in turn target the gene PIK3R3, slowing down cancer cell growth. Another gene, STMN1, was also found to be targeted by different microRNAs, resulting in reduced cell growth and a delayed cell cycle.

Senior authors Associate Professor Michael Michael and Professor Janni Petersen emphasized that these findings enhance our understanding of how metformin disrupts the growth of cancer cells. They noted that this research underscores the potential of metformin as a preventive agent against colorectal cancer and highlights the emerging promise of RNA therapeutics. These discoveries open new avenues for exploring the clinical efficacy of targeting specific microRNAs or pathways with RNA-based therapies to treat cancer.

The next phase of this research will involve focusing on the specific cellular pathways affected by metformin, which will pave the way for subsequent animal studies and eventually human clinical trials. This progression aims to validate the therapeutic benefits of targeting particular microRNAs or pathways, potentially leading to novel, targeted cancer treatments that could significantly improve patient outcomes.