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. 2020 Mar 30;24(6):370–378. doi: 10.29252/ibj.24.6.365

Fig. 4.

Fig. 4

Cisplatin enhancement by chemoresistance through EGFR/MEKK pathway. The SKOV3 (A) and OVCAR3 (B)  cell lines were treated with cisplatin (0.1 μg) and erlotinib (2 μM) for 48 h, then total RNA was harvested for qRT- PCR analysis. Erlotinib/cisplatin combination significantly reduced MDR genes in both cell lines with respect to the control. (C) SKOV3 cells were exposed to cisplatin (0.1 μg) as an igniter of chemoresistance, erlotinib (2 μM) as an anti-EGFR, bay11-7082 (5 μM) as an anti-NFκB, buparlisib (1 μM) as an anti-PI3K, and trametinib (5 μM) as an anti-MEKK1/MEKK2 for signaling dissection. After 48 h, RNA was harvested for qRT-PCR. HB-EGF (EGFR ligand) was evaluated in the treated cells