Fig. 3: Pharmacological inhibition of ILK and EGFR signaling confirmed the synergistic effects with FGFR inhibition. | Oncogenesis

Fig. 3: Pharmacological inhibition of ILK and EGFR signaling confirmed the synergistic effects with FGFR inhibition.

From: A functional CRISPR/Cas9 screen identifies kinases that modulate FGFR inhibitor response in gastric cancer

Fig. 3: Pharmacological inhibition of ILK and EGFR signaling confirmed the synergistic effects with FGFR inhibition.

Overexpression of FGFR2 was detected in KatoIII, SNU16, YCC28, and YCC30 cells by western blot. FGFR2 (#11835) and GAPDH (#5174) antibodies were purchased from Cell Signaling. Gastric cancer cell lines KatoIII and SNU16 were purchased from ATCC, and YCC-28 and YCC-30 were kindly provided by Dr. Sun Young Rha at Song-dang Institute for Cancer Research (Yonsei University, Seoul, Korea). Cells were cultured in IMDM supplemented with 20% FBS or RPMI-1640 supplemented with 10% FBS. Cell viability of KatoIII (b), SNU16 (c), YCC28(d), and YCC30 (e) were measured by CellTiter-Glo after treated with Cpd22 and lapatinib alone or in combination with AZD4547 for 96 h. The data are measured in hextuple or quintuple and displayed as mean ± s.e.m. ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05. The P values were calculated by Dunnett’s multiple comparisons test

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