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Fig. 4 | Cancer Cell International

Fig. 4

From: Markers of MEK inhibitor resistance in low-grade serous ovarian cancer: EGFR is a potential therapeutic target

Fig. 4

Cell signaling effects of selumetinib and erlotinib treatments in four MEKi-Re LGSC cell lines. As previously described, 24 h selumetinib treatment caused an increased in the levels of EGFR phosphorylation (p-EGFR Y1068) in 3 out of 4 MEKi-Re cell lines (VOA-6406, VOA-3723, and VOA-4627). As expected, erlotinib alone inhibited EGFR phosphorylation (p-EGFR Y1068) in all cell lines. Interestingly, erlotinib also inhibited MAPK phosphorylation (p-ERK1/2) in 2 out of 4 lines (VOA-3723 and VOA-4627), and increased it in another line (VOA-6406). No unique pathway interaction patterns for each of the MEKi-Re lines that were sensitive (VOA-6406, VOA-3723) or resistant (VOA-4627, VOA-3993) to erlotinib and selumetinib combination was detected

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