Several studies show that treatment with metformin, a drug used for the treatment of type 2 diabetes, reduces the risk of developing cancer. Classically, metformin acts in the liver decreasing glycemia and improving secondary hyperinsulinemia. Such effects could also impact tumorigenesis, since hyperinsulinemia has been associated with poor prognosis in several types of cancer, such as breast, colon and prostate. Also, numerous studies showed that the drug has a direct effect on neoplastic cells, but not all mechanisms are established. The mTOR pathway is possibly the most important route in the antineoplastic effect of metformin. Inhibition of mTOR alters protein synthesis and consequently the proliferation of tumor cells. The mTOR pathway is regulated by AMPK, which is an important regulator of the functions of T cells and inhibits the production of effector T lymphocytes and promote the generation of memory T cells. Our objective is to evaluate if targeting AMPK pathway in T lymphocytes can alter tumor incidence, tumor growth and metastasis, as well as to understand what are the effector immune mechanisms involved in this process.
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