Fig 1: EGFR/MET participated in regulation of phosphorylation of hetero-RTKs.A Western Blot was used to observe phosphorylation of RTKs in HCCLM3, MHCC97H and PLC/PRF/5 cell lines with Lenvatinib or Sorafenib added. B Western blot was used to determine the effect of down-regulation of EGFR/MET on hetero-RTKs, including: Phosphorylation of EGFR, MET, Her3, RON, IR/IGF-1R and RET in HCC cell lines with EGFR/MET inhibitor added. C Phosphorylation of EGFR, Her3, RON, IR/IGF-1R and RET in HCC cell lines with MET knock-down. D Phosphorylation of FGFR1, VEGFR2 and PDGFRß with ligand stimulated in HCC cell lines with EGFR/MET inhibitor added. E Phosphorylation of FGFR1, VEGFR2 and PDGFRß with ligand stimulated in HCC cell lines with MET knock-down. F Phosphorylation of RTKs in PLC/PRF/5 cell line with EGFR or MET knock-down.
Fig 2: miR-592 mimic abolishes the effect of ERBB3 overexpression on migration, invasion and colony formation in EOC cells. (A) Kaplan–Meier survival curves of patients with EOC at high and low ERBB3 expression in the Kaplan–Meier Plotter database. (B) SKOV3 cells were transfected with ERBB3 or/and miR-592 mimic. CCK-8 assay was used to measure cell viability in SKOV3. **P < .01. (C and D) Colony formation assay was conducted to assess SKOV3 cell proliferation. *P < .05; ***P < .001. Transwell assay was performed to assess cell migration (E and F) and invasion (G and H) in SKOV3 cells transfected with ERBB3 or/and miR-592 mimic. *P < .05; **P < .01; ****P < .0001. Values represent the means ± SD for three separate experiments.
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