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. 2024 Jul 22;115(10):3333–3345. doi: 10.1111/cas.16292

FIGURE 2.

FIGURE 2

The AXL inhibitor sensitized AXL‐overexpressing EGFR‐mutant NSCLC cells to lazertinib. (A) EGFR‐mutant NSCLC cell lines PC‐9, HCC4011, H1975, PC‐9GXR, KPP‐03, HCC827, and HCC4006 were lysed, and the indicated proteins were detected using western blotting. (B) EGFR‐mutant NSCLC cell lines PC‐9, HCC4011, H1975, and KPP‐03 were incubated with lazertinib (100 nmol/L) or a combination of lazertinib (100 nmol/L) and AXL inhibitor ONO7475 (100 nmol/L) for 72 h. Cell growth was determined using MTT assays. *p < 0.05. (C) Quantitative determination of the inhibition of cell viability of high‐AXL‐expressing and low‐AXL‐expressing EGFR‐mutant cells treated with the EGFR‐TKI lazertinib (100 nmol/L) in the presence or absence of ONO7475 (100 nmol/L) for 72 h. Paired Student's t‐tests were used for comparisons. (D) PC‐9 and HCC4011 cells were treated with lazertinib (100 nmol/L), ONO7475 (100 nmol/L), or a combination of lazertinib and ONO7475 for 4 h. (E) PC‐9 and HCC4011 cells were treated with lazertinib (100 nmol/L), ONO7475 (100 nmol/L), or a combination of lazertinib and ONO7475 for 72 h. (F) PC‐9, HCC4011, and H1975 cells were visualized using crystal violet staining following 9 days of treatment with lazertinib (100 nmol/L), ONO7475 (100 nmol/L), or a combination of lazertinib and ONO7475 where the drugs were replenished every 72 h. (G) PC‐9, HCC4011, and H1975 cells were treated with lazertinib (100 nmol/L), ONO7475 (100 nmol/L), or a combination of lazertinib and ONO7475 in which the drugs were replenished every 72 h. Absorbance was measured every 3 days. *p < 0.05.