FIGURE 7.

KRAS mutations suppress B2M expression in lung cancer. (a) Cell viability assay for H358 and H23 cells treated with ARS‐1620 at various concentrations for 96 h. (b,c) FACS analysis of B2M on the surface of H23 and H358 cells treated with AMG510 for 24 h. (d) Western blot demonstrating the levels of p‐ERK, ERK and B2M, with β‐catenin as a loading control. (e,f) Real‐time PCR results indicating B2M transcription upon AMG510 treatment for 24 h in H358 and H23 cells. (g) Mutant KRAS^G12V was introduced into the BEAS‐2B normal bronchial epithelial cell line, and B2M transcription was assessed by real‐time PCR. (h) Western blot showing the reduced B2M in BEAS‐2B cells overexpressing KRAS^G12V. (i–j) GSEA of the RNA‐seq results and the top 10 upregulated pathways upon treatment with ARS‐1620. (k) Tumour volumes of H358 xenografts in mice treated with AMG510 or vehicle (n = 5). (l) IHC staining for B2M in H358 xenografts treated with AMG510 or control (**p < 0·01 vs. control)