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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Inhibiting the glycerophosphodiesterase EDI3 in ER-HER2+ breast cancer cells resistant to HER2-targeted therapy reduces viability and tumour growth

Fig. 1

EDI3 expression and enzyme activity according to HER2 and ER status. A, EDI3 (GPCPD1; 224826_at) mRNA expression was compared among subtypes defined according to HER2 and ER status in human breast cancer Affymetrix datasets (total n = 540). B, EDI3 protein expression in breast cancer subtypes using IHC on a TMA (n = 265); high expression was defined as strong positivity in > 50% of tumour cells, intermediate as weak in >50% or strong in ≤ 50% of tumour cells, and low as negative or weak in ≤ 50% of tumour cells. C, qPCR analysis of EDI3 mRNA expression in a panel of breast cancer cell lines of different molecular subtypes normalized to β-Actin. D, Representative Western blot (left panel) showing pHER2, HER2, EDI3 and ERα protein expression in the panel of breast cancer cell lines, with quantification normalized to β-Actin (right panel). E, EDI3 enzyme activity measured using an enzyme-coupled assay that indirectly measures the release of choline. F, Intracellular PCho/GPC ratio measured using NMR spectroscopy. Cell line data (C-F) are mean ± SD of at least three independent experiments. IHC, immunohistochemistry; TMA, tissue microarray; NMR, nuclear magnetic resonance

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