Introducing in silico based strategies for modeling and predicting proteinprotein interactions involved in anticancer mechanisms of actions of metformin against thyroid carcinoma

Thyroid cancer is the utmost common endocrine malignancy with more deaths yearly than all other endocrine cancers combined. Considering the incidence of thyroid cancer, so far different treatments have been carried out, such as surgery, radioiodine treatment, chemotherapy and hormone treatment. For this purpose, new therapies and drugs are under development to treat cancer and reduce the risk of chemotherapy drugs. Metformin, a well-known insulin-sensitizer typically utilized for type ۲ diabetes therapy, has lately identified as potentially drug in oncology. On the cellular level, it exerts an antimitogenic property via induction of the AMP-activated protein kinase (AMPK) and by inhibition of the MAPK pathway as the main part of insulin/IGF signaling with regulatory role in the cell growth process.This dual mode of metformin action can introduce it as a potential drug for anticancer thyroid therapy. An interesting part of investigations in thyroidology is the recently introduced association of insulin resistance with thyroid functional and morphological abnormalities. Consequently, patients treated with metformin have a smaller thyroid volume and a lower risk of cancer. Numerous researches have suggested that metformin can inhibit the growth of thyroid cells by affecting the insulin/IGF۱ and mTOR pathways in vitro and in vivo. Based on this evidence, metformin appears to be a promising therapeutic tool in patients with thyroid disease. Despite the mentioned research and relevant results, as yet the mechanisms underlying the antitumor effect of metformin against thyroid carcinoma are complex and still not fully understood.

کلیدواژه ها:

In silico ، Thyroid carcinoma ، metformin ، String