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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Mol Cancer Ther. 2015 Jul 30;14(10):2313–2320. doi: 10.1158/1535-7163.MCT-14-1071

Figure 4. miR-124 modulates the ESX/EGFR axis to potentiate the anti-tumor efficacy of EGFR/Her2 TKIs.

Figure 4

(a) Restoration of miR-124 potentiates the activity of afatinib and lapatinib. SCC15/miR-control and SCC15/miR-124 cells were treated with lapatinib or afatinib at the IC50 dose. Colonies were stained with crystal violet. Data is normalized to vehicle-treated SCC15/miR-control cells and presented as mean ± SEM. *p<0.01, SCC15/miR-control vs. SCC15/miR-124 for vehicle, lapatinib, or afatinib, n=3. **p<0.01 SCC15/miR-124/vehicle, SCC15/miR-control/lapatinib or SCC15/miR-control/afatinib vs. SCC15/miR-124/lapatinib or SCC15/miR-124/afatinib, n=3. (b) Ectopic over-expression of EGFR in SCC15/miR-124 cells. Stable polyclonal SCC15/miR-124/vector and SCC15/miR-124/EGFR cells were generated by antibiotic selection. Whole cell lysates were extracted and immunoblot analyses were performed for EGFR, STAT3 and pSTAT3. (c) Recapitulation of EGFR in SCC15/miR-124 cells promotes resistance to EGFR/Her2 TKIs. SCC15/miR-control, SCC15/miR-124/vector and SCC15/miR-124/EGFR cells were treated with lapatinib or afatinib at the IC50 dose. Colonies were stained with crystal violet. Data is normalized to vehicle-treated SCC15/miR-control cells and presented as mean ± SEM. *p<0.01, SCC15/miR-124/vector vs. SCC15/miR-124/EGFR for vehicle, lapatinib, or afatinib, n=3.