Metformin slows the growth of colorectal cancer cells
最近審查：14.06.2024
所有iLive內容都經過醫學審查或事實檢查，以確保盡可能多的事實準確性。
我們有嚴格的採購指南，只鏈接到信譽良好的媒體網站，學術研究機構，並儘可能與醫學同行評審的研究相關聯。 請注意括號中的數字（[1]，[2]等）是這些研究的可點擊鏈接。
如果您認為我們的任何內容不准確，已過時或有疑問，請選擇它並按Ctrl + Enter。
A new study has examined what happens when the type 2 diabetes drug metformin is used to treat colon cancer cells, showing that it could be used to develop new cancer treatments. The work was published in Cancers magazine.
Previous epidemiological studies suggest that taking metformin helps protect patients with diabetes from developing some forms of cancer, including colon cancer.
Researchers from Flinders University were trying to understand how taking the drug metformin affects cancer cells and how it could help in future cancer treatments.
“Using the latest techniques, we analyzed how metformin helps stop the growth and proliferation of colon cancer cells by controlling specific 'pathways' within cells that regulate growth and division,” says lead author Dr Ayla Orang from the School of Medicine and Faculty Flinders University Public Health
"Importantly, our work revealed that metformin uses small pieces of RNA (called microRNAs) to act as a 'switch' and turn off certain genes that are involved in cell growth and division, so our findings could later be used to development of new targeted cancer therapy.
"Specifically, we found that metformin increases the levels of certain microRNAs, such as miR-2110 and miR-132-3p, which then target specific genes and slow the growth and progression of tumors. With this information, we can develop therapies RNA-based are new cancer treatments that target RNA molecules (such as microRNAs)," she says.
The study, "Restricting Colon Cancer Cell Metabolism by Metformin: An Integrated Transcriptomic Study," used advanced techniques to study microRNAs and the full range of gene expression in colon cancer cells to help understand how metformin affects cells. p>
Metformin increased the levels of certain microRNAs (miR-2110 and miR-132-3p) targeting a specific gene (PIK3R3).
This process helps slow the growth of cancer cells and prevent them from multiplying too quickly. Another gene (STMN1) was also targeted by various microRNAs, resulting in decreased cell growth and cell cycle arrest.
The paper's co-authors, Senior Associate Professor Michael Michael and Professor Janni Petersen, say the findings are a step forward in our understanding of how metformin disrupts the growth of cancer cells and how it could be used to fight cancer.
"Our research provides new insights into the molecular mechanisms of metformin's action and how we can target the genes responsible for turning normal cells into cancer cells," says Associate Professor Michael.
"This is important because it shows the potential of metformin as a preventive agent to reduce cancer growth in the colon, and the emergence of RNA therapy as a promising new avenue to study the clinical effectiveness of these findings. We need to further explore the potential therapeutic benefits of targeting specific microRNAs or pathways using RNA therapy to treat cancer.
"After using metformin to uncover metabolism in cancer cells, the next stage of research will be to focus on specific cellular pathways, leading to animal studies and then clinical studies in humans."