Fig. 6: EGFL7-mediated activation of NOTCH signaling buffers EGFR kinase inhibition. | Cell Death & Disease

Fig. 6: EGFL7-mediated activation of NOTCH signaling buffers EGFR kinase inhibition.

From: EGFL7 drives the evolution of resistance to EGFR inhibitors in lung cancer by activating NOTCH signaling

Fig. 6: EGFL7-mediated activation of NOTCH signaling buffers EGFR kinase inhibition.The alternative text for this image may have been generated using AI.

A Western bolt analysis showing the levels of EGFR, pEGFR, the first cleaved product (NTM) and active form (NCID) of NOTCH1 as well as EGFL7 in PC9 cells treated with 1 µM osimertinib (Osm) for the indicated time points. B Western bolt analysis showing the levels of EGFR, pEGFR, NOTCH1-NTM, NOTCH1-NCID, c-Myc and EGFL7 in EGFL7-knockdown PC9 cells and control cells treated with 1 µM osimertinib (Osm) for the indicated time points. GAPDH was used as a loading control. C Survival curves of PC9 cells treated with a combination of different concentrations of osimertinib (Osm) and vehicle control (DMSO) or NOTCH signaling inhibitor dibenzazepine (DBZ) for 72 h. Data present as average of four identically wells of percentage of surviving cells to vehicle-treated control. D Western blot analysis showing the levels of change of EGFR, pEGFR, NOTCH1-NCID, c-Myc, pERK and ERK1/2 in PC9 cells treated with the indicated treatments. GAPDH was used as a loading control. E, F Heat maps presenting the normalized enrichment score of the indicated gene sets in the indicated experiments when the NOTCH signaling was activated or repressed (see methods). Data are shown as mean ± SEM. p values are calculated by unpaired two-tailed Student’s t test (**p < 0.01; ***p < 0.001).

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