miR-206 contributed to euthyrox resistance in PTC cells through blockage p38 and JNK signaling pathway by targeting MAP4K3, providing a potential therapeutic application for the treatment of patients with euthyrox-resistant PTC in the further.
In addition, Ad/sh-NOB1 combined with DOX treatment significantly increased activation of the p38 MAPK pathway, which may contribute to inhibition of PTC cell growth and decreased DOX resistance.
Moreover, our results also showed that downregulation of NOB1 was able to significantly activate constitutive phosphorylation of p38 MAPK, which might contribute to the inhibition of PTC cell growth.