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. 2013 Dec;15(12):1354–1362. doi: 10.1593/neo.131660

Figure 4.

Figure 4

RSK3 is activated by EGF/EGFR through the MEK/ERK signaling cascade and modulates rpS6 phosphorylation. Serum-starved cells were incubated with the EGFR inhibitor erlotinib, the MEK inhibitor UO126, or the PI3K inhibitor LY294002 for 2 hours before stimulation with EGF for 15 minutes. Phosphorylation status of ERK and RSK3 (A) as well as rpS6 (B) was determined using specific antibodies by Western blot analysis in PaTu-8988t cells harboring mutant KRAS. (C and D) BxPC-3 cells with wild-type KRAS (Mock) and BxPC-3 cells stably transfected with constitutively active KRAS (KRAS) were incubated with the indicated compounds as above. Phosphorylation status of ERK and RSK3 (C) as well as rpS6 (D) was determined using specific antibodies by Western blot analysis in BxPC-3 cells stably expressing wild-type (Mock) or mutant KRAS (KRAS). Note that the PI3K inhibitor LY294002 has a profound impact on rpS6 phosphorylation but not on RSK3 phosphorylation, suggesting that PI3K/mTOR signaling affects rpS6 phosphorylation independently of RSK3.