In breast cancer, alteration of miR-145 expression has also been frequently reported23–26, but only a few studies have investigated its upstream signaling pathways (e.g., MTH1, an enzyme, is capable of hydrolyzing the oxidized dNTPs and NTP, such as 8-oxo-dGTP and 2-OH-dATP, to form and prevent their incorporation into the nucleus and mitochondrial DNA to limit reactive oxygen species [ROS] production for induction of cell damage)27,28. This evidence concerns the gene NUDT1 and breast carcinoma.