Fig. 2
From: p65BTK is a novel potential actionable target in KRAS-mutated/EGFR-wild type lung adenocarcinoma
NSCLC cells with activated KRAS express high levels of p65BTK. a Top: Western Blot analysis of p65BTK expression in NSCLC human cell lines with different mutations along the RAS/MAPK pathway and in p53. Lysate from HCT116p53KO colon cancer cells was loaded as a positive control. Bottom: fold change of p65BTK protein expression in NSCLC cell lines normalized to beta actin, setting as expression level = 1 NCI-H1935 which do not possess mutations in KRAS or in the RAS/MAP pathway not in the p53 gene. b Top: Western Blot analysis of p65BTK expression in primary lung cancer cells derived from KrasLSL-G12D (LKR10, LKR13, LSZ1) and KrasLSL-G12D;Trp53f/f (389 N1, 482 N1) mice. UNSCC680 is a primary cell line from a mouse squamous cell carcinoma. Bottom: fold change of p65BTK protein expression normalized to beta actin. In a and b p65BTK was detected by BN49 antibody [18] and beta actin was used as a loading control. c IHC analysis of p65BTK in normal and tumoral lung tissue samples from 2 different KrasLSLG12D; Trp53 f/f mice using BN30 antibody. d Left: Western Blot analysis of p65BTK expression in SK-Lu-1 and NCI-H2228 cells after treatment with the MEK inhibitor Trametinib (1 μM). Right: fold change of p65BTK protein expression normalized to vinculin