Metformin impairs cisplatin effects in cell size and proliferation of A549 lung cancer cells, modulating the mTOR and other metabolic pathways.

Lung cancer is the leading cause of cancer death worldwide and reports innate and acquired therapeutic resistance to cisplatin. Metformin (MET), an antidiabetic agent with potential antitumor activity, overcomes cisplatin resistance in some cancers through AMPK-dependent and independent mechanisms. MET is a potential treatment in cells with LKB1 mutation, even with the impairment of AMPK and overactivation of mTOR signaling. The present study investigated the role of mTOR signaling and other signaling pathways after MET treatment in control and resistant A549 cells, mapping pathways and possible targets for cisplatin sensitivity induced by metformin.