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Adelaide, Australia – In a groundbreaking study, researchers at Flinders University have uncovered how the commonly prescribed diabetes medication metformin could be leveraged to control the growth of tumors. This discovery opens up the possibility for designing more effective cancer treatments in the future.
The study focused on the effects of metformin on colorectal cancer cells, demonstrating its potential as a tool for developing new cancer therapies. Epidemiological data has previously indicated that metformin usage in diabetes patients correlates with a reduced risk of developing certain cancers, including colorectal cancer.
Dr. Ayla Orang, the lead author from Flinders University’s College of Medicine and Public Health, explained the innovative approach taken in this research. “Using the latest techniques, we analyzed how metformin helps to stop colorectal cancer cells from growing and multiplying by controlling certain ‘pathways’ inside the cells that regulate growth and division,” she said.
The key finding of the study is that metformin increases levels of specific microRNAs, such as miR-2110 and miR-132-3p. These microRNAs act as ‘circuit breakers’ that turn off genes involved in cell growth and division. By doing so, they slow down the progression and proliferation of cancer cells.
“Our research has pinpointed that metformin uses small pieces of RNA to target specific genes, slowing down tumor growth,” Dr. Orang noted. “This discovery could eventually lead to the development of new targeted cancer therapies, particularly RNA-based treatments that focus on microRNAs.”
The study, titled “Restricting Colorectal Cancer Cell Metabolism with Metformin: An Integrated Transcriptomics Study,” utilized advanced techniques to analyze microRNAs and the full set of genes expressed in colon cancer cells. The findings showed that metformin increased the levels of microRNAs that target the gene PIK3R3, thereby slowing cancer cell growth. Another gene, STMN1, was also affected, leading to delayed cell cycle progression.
Senior authors Associate Professor Michael Michael and Professor Janni Petersen emphasized the significance of these results. “Our research provides new insights into the molecular mechanisms of how metformin works and how we might target genes responsible for turning normal cells cancerous,” said Associate Professor Michael. “This is crucial as it highlights metformin’s potential as a preventive agent for reducing bowel cancer growth and supports the promise of RNA therapeutics.”
The next steps in this research involve focusing on specific cell pathways, which will eventually lead to animal studies and human clinical trials. This progression is essential for determining the therapeutic benefits of targeting specific microRNAs or pathways with RNA-based therapies in cancer treatment.
This study represents a significant advancement in understanding how metformin disrupts cancer cell growth, potentially paving the way for innovative and effective cancer therapies in the future.
