MED12 mutation activates Notch signaling to enhance cancer stemness and suppress CD8+ T cell cytotoxicity in lung cancer

Figure 3 Mediator complex subunit 12 mutation maintained cancer stem cell properties via the Notch signaling pathway. A: Chromatin immunoprecipitation-quantitative polymerase chain reaction analysis of mediator complex subunit 12 occupancy at the HES1 promoter in lung cancer cells; B: Western blot was performed to detect NOTCH1, N1ICD, HES1, and HEY1 protein expression in NCI-H322 and PC9 cells; C: Flow cytometry was used to examine the apoptosis rates of NCI-H322 and PC9 cells treated with or without DAPT; D: Sphere formation assay was used to evaluate the sphere-forming ability of NCI-H322 and PC9 cells treated with or without DAPT; E: Flow cytometry was used to analyze the percentage of ALDH1-positive cells in NCI-H322 and PC9 cells treated with or without DAPT. Data are presented as mean ± SD. All experiments were repeated 3 times. ^aP < 0.05, ^cP < 0.001. NS: Not significant; MED12: Mediator complex subunit 12; IgG: Immunoglobulin G.