Metformin exerts an antitumoral effect on papillary thyroid cancer cells through altered cell energy metabolism and sensitized by BACH1 depletion.

In conclusion, metformin exerts an antitumoral effect on PTC cells both in vitro and in xenograft mouse models. A possible mechanism is through inhibiting glucose metabolism and mitochondrial respiration process. Knocking down BACH1 caused the switching of energy metabolism and sensitized PTC cells to metformin, which eventually enhanced the anti-tumor effect of metformin.