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. Author manuscript; available in PMC: 2019 Jan 22.
Published in final edited form as: J Invest Dermatol. 2017 Jun 7;137(10):2187–2196. doi: 10.1016/j.jid.2016.12.033

Figure 2. p90RSK inhibition is an effective therapeutic strategy in dual-resistant melanoma lines.

Figure 2.

RSK inhibitor treatment with (a) BI-D1870 or (b) BRD 3789 results in significant growth inhibition in both drug-naïve and acquired BRAF/MEK-inhibitor-resistant lines over 72 hours alone or in combination with vemurafenib and selumetinib. Growth inhibition with vemurafenib and selumetinib alone (no RSK inhibitor) plotted for comparison in green with error bars at 0 μM RSK inhibitor concentration. Mean ± SEM, N = 3. (c) Western blotting for signaling nodes involved in translation with 24-hour 5 μM BI-D1870, 5 μM vemurafenib, and 150 nM selumetinib triple therapy shows significant downregulation over dual Vem + Sel therapy alone. (d). shRNA-mediated knockdown of RSK1 and RSK2 leads to significant growth inhibition of YUMACdr treated with 5 μM vemurafenib and 150 nM selumetinib over 72 hours, P < 0.0001, mean ± SEM, N = 3. MEK, MAPK/ERK kinase; p90RSK, p90 subfamily of ribosomal S6 kinase; RPS6, ribosomal protein S6; SEM, standard error of the mean.