MKNK2is A Valid Target Of MiR-125b In Breast Cancer

It has been shown that MKNK2is increased and continuously activated in HER2-overexpressing cells. MKNK2phosphorylates and activates eIF4E, a rate limiting factor in protein synthesis which enhances the translation of some oncoproteins involved in cell cycle, apoptosis and angiogenesis regulation. However, the knowledge about how MKNK2mediate tumor development is limited. In this study, we found that the expression of miR-125b are inversely correlated with the levels of MKNK2, but no relationship was found with either tumor stages or Her2status, in human breast cancer development. We showed that miR-125b inhibited tumor cell growth and invasion by regulating MKNK2at posttranscriptional level. Thus, both miR-125b and MKNK2could be therapeutically targeted in breast cancer.