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

FIGURE 6.

FIGURE 6

Inhibition of YAP via downregulation of MCL‐1‐sensitized EGFR‐mutant NSCLC cells to lazertinib and AXL inhibitor. (A) PC‐9 and HCC4011 cells were treated with lazertinib (100 nmol/L) with or without ONO7475 (100 nmol/L) and YAP inhibitor verteporfin (1 μmol/L) for 48 h. The cells were lysed, and the indicated proteins were detected using western blotting. (B) qPCR of MCL‐1 in PC‐9 and HCC4011 cells treated with lazertinib (100 nmol/L) and ONO7475 (100 nmol/L) with or without verteporfin (1 μmol/L) for 48 h. *p < 0.05. (C) PC‐9 and HCC4011 cells were treated with lazertinib (100 nmol/L) with or without ONO7475 (100 nmol/L) and verteporfin (1 μmol/L) for 72 h. Cell growth was determined using MTT assays. *p < 0.05. (D) PC‐9 and HCC4011 cells were visualized using crystal violet staining following 9 days of treatment with lazertinib (100 nmol/L), ONO7475 (100 nmol/L), verteporfin (1 μmol/L), or combinations, with the drugs replenished every 72 h. (E) PC‐9 and HCC4011 cells were treated with lazertinib (100 nmol/L) with or without ONO7475 (100 nmol/L) and verteporfin (1 μmol/L) for 48 h. The cells were lysed, and the indicated proteins were detected using western blotting. (F) Schematic presentation of the mechanism by which a combination of lazertinib and ONO7475 promote the YAP–MCL‐1 axis and facilitate the synthesis of antiapoptotic proteins in EGFR‐mutant NSCLC cells.