Fig. 3: GAS6–AXL axis-induced drug-tolerant cells with HER2-TKIs. | npj Precision Oncology

Fig. 3: GAS6–AXL axis-induced drug-tolerant cells with HER2-TKIs.

From: AXL–SHC1 signaling axis mediates adaptive resistance to HER2-targeted tyrosine kinase inhibitors in HER2-aberrant lung and gastric cancers

Fig. 3: GAS6–AXL axis-induced drug-tolerant cells with HER2-TKIs.The alternative text for this image may have been generated using AI.

A qPCR analysis of GAS6 expression in Calu-3 and MKN7 parent cells treated with nonspecific (control) or GAS6-specific siRNAs for 48 h. *P < 0.05 (unpaired t-tests). B MTT assays evaluating cell viability of Calu-3 and MKN7 cells treated with nonspecific or GAS6-specific siRNAs were incubated with or without mobocertinib (0.01 or 0.1 μmol/L) for 72 h. These cell lines were incubated in an RPMI 1640 medium with 0.1% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 μg/mL) in a humidified 5% CO2 incubator at 37 °C for 72 h (*P < 0.05, one-way ANOVA). C Western blotting analysis of Calu-3 and MKN7 cells transfected with nonspecific or GAS6-specific siRNAs for 48 h, followed by treatment with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h. D Calu-3 and MKN7 cells with nonspecific siRNA or AXL-specific siRNAs were treated for 72 h with or without mobocertinib (0.01 or 0.1 μmol/L) and/or GAS6 (50 ng/mL). Cell growth was determined using MTT assays. *P < 0.05 (two-way ANOVA). E Western blotting of Calu-3 and MKN7 cells transfected with nonspecific or AXL-specific siRNAs and treated with or without mobocertinib (0.01 or 0.1 μmol/L) for 4 h and GAS6 (50 ng/mL) for 15 min. F MKN7 cells treated with or without mobocertinib (Mobo, 0.1 μmol/L) for 24 h were detected by western blotting with immunoprecipitation of the indicated proteins.

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