IQGAP1 promotes tumor progression by stabilizing MCM3/Nrf2 in cholangiocarcinoma

Figure 5 IQGAP1 promoted the progression of cholangiocarcinoma by mediating the MCM3/Nrf2 axis. A: The altered protein amount of MCM3 regulated by IQGAP1 could be terminated by the addition of the proteasome inhibitor MG132; B: The addition of actinotide inhibited intracellular protein synthesis and faster degradation of MCM3 was observed upon knockdown of IQGAP1, and the addition of actinotide inhibited intracellular protein synthesis and lower degradation of MCM3 was observed upon overexpression of IQGAP1; C: IQGAP1 prevented MCM3 degradation through ubiquitin-dependent breakout; D: The deubiquitination of MCM3 mediated by IQGAP1 could be reversed by USP28 knockdown; E and F: MCM3 regulated by IQGAP1 competitively bound Nrf2 to KEAP1, resulting in a positive correlation between the expression of Nrf2 and the change of MCM3; G: Dihydroethidium staining of cells assessed oxidative stress levels; H: Flow cytometry was used to detect apoptosis. NC: Negative control; OE: Overexpression; si: Silence; UB: Ubiquitination; IP: Immunoprecipitation.