Fig. 7
Vitamin C inhibit the feedback activation of MAPK/ERK pathways in a ROS dependent way. a The indicated cells were treated with PLX4032 4 μM, Vitamin C 0.5 mM (VC) with or without NAC 0.5 mM for 24 h, and cell lysates were then subjected to western blot analysis to determine the re-activation of MAPK/ERK pathways (upper panels). The normalized band intensity of Pan-AKT and pERK were shown in lower panels, tERK was used for normalizing pERK. b Treating BRAFMT thyroid cancer with simple PLX4032 will induce a feedback activation of MAPK/ERK as well as PI3K/AKT pathways, leading to the drug resistance and cell survival. c When we combined Vitamin C and PLX4032, the feedback activation was inhibited by Vitamin C due to the accumulation of ROS, leading to the death of cancer cells. Data were presented as mean ± SD. ns, not significant; ***/^^^/###, P < 0.001. ns: compared with control group; *: compared withPLX4032 + VC group; ^: compared with VC group; #: compared with PLX4032 group