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. 2019 Aug 15;21(10):945–962. doi: 10.1016/j.neo.2019.07.002

Figure 4.

Figure 4

SMAR1 increases MHC I expression on cancer cells. (a and b) HCT116 p53+/+ cells were lysed and immunoprecipitation studies were carried out to check the interaction between calnexin and MHC I. IP was performed with α-calnexin and α-HLA ABC antibodies. Western blot analysis was done and blots were probed with α-calnexin and α-HLA ABC antibodies. (c) HCT116 p53+/+ cells were transfected with flag-vector and flag-SMAR1 constructs. Cells were harvested after 48 h and stained with PE-HLA ABC (MHC I) antibody. Flow cytometry acquisition was done with FACS calibur. (d) Flow cytometry was done with HCT116 p53+/+ cells transfected with flag-vector or flag-SMAR1 constructs, treated with 100 nM trichostatin A and stained with PE-HLA ABC (MHC I) antibody. Real-time PCR was done to check the relative gene expression of ERAP1 in (e) HCT116 p53+/+ and HCT116 p53−/− cells after SMAR1 overexpression. GAPDH was used as endogenous control.