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Fig. 5 | Genome Medicine

Fig. 5

From: Secondary resistance to anti-EGFR therapy by transcriptional reprogramming in patient-derived colorectal cancer models

Fig. 5

Functional analysis of the PPP2R5A R112L mutation. a, b qRT-PCR and western blot data confirming the overexpression of either the wt or the R112L mutant PPP2R5A transgene. c Relative quantification of the indicated protein signal intensities to the corresponding intensities of the control tumor normalized with the corresponding GAPDH signal intensities using Image Lab (BioRad). d Proliferation response of colon cancer cells BoC20 and DiFi overexpressing either the wt or the R112L mutant version of PPP2R5A with or without CET treatment (DiFi: CET 0.4 μg/ml; BoC20: CET 5 μg/ml). e Western blot analysis of pEGFR, pAKT, and pERK following stimulation of serum-starved (0.1% FCS) cells with hEGF (200 ng/ml) for the indicated time. pSFFV-GFP vector transduced cells were used as controls. GAPDH was used as the loading control

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