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. 2020 Mar 2;12(4):e11177. doi: 10.15252/emmm.201911177

Figure 4. Oncogenic EphA2 signaling switch is associated with platinum resistance and mediated by treatment‐activated ERK1/2‐RSK axis in OC cells.

Figure 4

  • A, B
    Immunoblot images show EphA2 (A; total, pS897, and pY588) and corresponding pS897/pY588 ratios (B) of TYK‐nu and TYK‐nu.R after treatment with 0–10 μM cisplatin for 72 h. N = 5.
  • C, D
    EphA2 (total and phosphorylated) in the cells treated (C) and untreated (D) with 0–80 μM carboplatin for 72 h.
  • E, F
    EphA2 (total and pS897) in TYK‐nu after treatment with inhibitors against MEK (UO126, 10 μM), PKA (H89.2HCl, 10 μM), PI3K (LY294002, 10 μM) or its alpha subunit (BYL‐719, 5 μM), and RSK (BI‐D1870, 10 μM) in combination with 0–10 μM cisplatin for 72 h (E). Corresponding EphA2‐pS897 quantification for BI‐D1870 treatment (F). N = 5.
  • G
    EphA2 (total and pS897) in TYK‐nu.R treated with 0–20 μM cisplatin without or with 10 μM BI‐D1870 for 72 h.
  • H, I
    EphA2, RSK, and ERK1/2 (total and phosphorylated) in TYK‐nu (H) and OVCAR4 (I) treated with 0–30 μM carboplatin without or with 50 μM LJH685 for 72 h.
Data information: In (B and F), data are presented as mean (SD). *P < 0.05, **P < 0.01. Exact P‐values are provided in Appendix Table S10, Student's t‐test.Source data are available online for this figure.