Analysis Of The Effects Of Metformin Administered Alone Or In Combined Treatments In Colorectal Cancer
Abstract
The aim of this project was to investigate the anticancer activity of the anti-diabetic drug metformin, individually or combined in various settings with chemotherapy, on in vitro models of colorectal cancer (CRC). I found that metformin reduced cell proliferation by inducing cell cycle arrest in the G0/G1 phase, but did not lead to cell death. The anti-proliferative action of metformin resulted mediated by the inactivation of the mTOR pathway and of IGF1R protein. However, the drug only transiently arrested cell growth, since its effects were reversed after drug removal. When I combined the biguanide with the chemotherapy drugs commonly used to treat CRC I observed different responses in the cell lines analysed that reflected their genetic background and their different sensitivities to both the biguanide and chemotherapy. I found that metformin added before chemotherapy drugs antagonised their effects in the majority of the treatments. On the contrary, its administration after long chemotherapeutic treatments significantly reduced the cell viability. I noted that metformin better inhibits cell proliferation in cell lines with rapid growth. I have also assessed the dual treatment combination of metformin with different drugs that target specific genes or proteins (targeted therapies), focusing on BRAF-mutant cell lines. For most of the tested treatments the simultaneous administration of metformin and target drugs gave no advantages over the single drugs, and often resulted…
How strong is the evidence?
Evidence Hub reads this as a thesis, done in cell cultures (in vitro), not in people. Its evidence level is 5 of 5 (Very low · case / narrative / animal / in vitro / in silico). Case reports, narrative reviews, and animal, cell or computer-model studies give the weakest evidence for human health.
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