Skip to main content
. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: Mol Cancer Res. 2015 May 1;13(8):1227–1237. doi: 10.1158/1541-7786.MCR-14-0183-T

Figure 3. In U87MG cells, SPRY2 knockdown reduces MKP-1 and MKP-5 mRNA expression, and MKP-1 or MKP-5 knockdown enhances cellular response to EGFR and c-MET co-inhibition.

Figure 3

(A) MKP-1, MKP-5, and MKP-3 mRNA levels were measured in U87MG dead kinase (DK) EGFRvIII cells expressing control shRNA or SPRY2-targeting shRNA (shRNA #1). (B) Whole cell lysates from U87MG DK or high (H) EGFRvIII cells expressing a control, MKP-1-targeting, or MKP-5-targeting shRNA were probed by western blot using antibodies against the indicated proteins, and blots were analyzed by densitometry. (C) The indicated cell lines were treated with DMSO or 10 µM gefitinib + 5 µM PHA665752 (G+P) for 48 hrs prior to flow cytometry analysis for ToPro3 permeability. Throughout the panels, data are represented as the average of three independent experiments ± s.e.m. Asterisks indicate p < 0.05, and “NS” indicates lack of statistical significance.