Journal: Cells

Article Title: Diverse Mechanisms of Resistance against Osimertinib, a Third-Generation EGFR-TKI, in Lung Adenocarcinoma Cells with an EGFR -Activating Mutation

doi: 10.3390/cells11142201

Figure Lengend Snippet: AZDR3 cells exhibit EGFR amplification and loss of EGFR exon 19 deletion, resulting in osimertinib resistance. ( a , b ) Western blot analysis of AZDR3, AZDR6, AZDR9 ( a ), and PC-9 ( b ) cells, following exposure to osimertinib for 24 h. ( c ) Cell viability following afatinib treatment for 72 h ( n = 6). ( d ) Western blot analysis of AZDR3, AZDR6, and AZDR9 cells, following treatment with afatinib for 24 h. ( e ) EGFR knockdown in AZDR3, AZDR6, and AZDR9 cells, following transfection with non-targeting (N/T) siRNA or siRNA directed against EGFR. ( f ) Dimensions of tumors from female severe combined immunodeficiency mice injected with PC-9 and AZDR3 cells ( n = 6) and treated with or without osimertinib (5 mg/kg) or afatinib (6 mg/kg). Data are presented as the mean tumor volume ± SEM; * p < 0.01. Cle-PARP, cleaved poly (ADP-ribose) polymerase.

Article Snippet: Six-eight-week-old female severe combined immunodeficiency (SCID) mice (strain: C.B-17/IcrHsd-Prkdcscid) were purchased from Sankyo Labo Service Corporation (Tokyo, Japan), housed, and treated according to institutional guidelines.

Techniques: Amplification, Western Blot, Knockdown, Transfection, Injection