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Figure 1 | Breast Cancer Research

Figure 1

From: A novel inhibitor of fatty acid synthase shows activity against HER2+ breast cancer xenografts and is active in anti-HER2 drug-resistant cell lines

Figure 1

G28UCM inhibits the growth of BT474 xenografts and do not induce weight loss in vivo. A. Daily i.p. 40 mg/Kg G28UCM-treatment decreased tumour volume in a BT474 breast cancer xenograft (n = 14, grey bars) compared to vehicle control (n = 9, white bars). Five G28UCM-treated animals exhibited no identifiable residual tumour at the end of the experiment (10T, 11T, 12T, 13T and 14T, grey bars). Data are expressed as logarithm of percentage of individual tumour growth at day 45 respect to day 0. B. G28UCM-treated tumours showed apoptosis and inactivation of HER2, ERK1/2 and mTOR signalling pathways, without affecting FASN protein expression levels. This figure only shows a representative animal of each experimental group (4C -control-, 4T -treated no-responsive- and 12T -responsive-). All tumours were lysed and equal amounts of protein were subjected to Western blot analyses with anti-PARP, anti-FASN, anti-HER2, anti-AKT, anti-ERK1/2 and anti-mTOR antibodies. Activation of the protein under study was analysed by assessing the phosphorylation status using the corresponding phospho-specific antibody. Blots were reprobed for β-actin as loading control. Gels shown are representative of those obtained from two independent experiments. C. FASN expression level does not change between control and G28UCM-treated animals. Representative immunohistochemical staining for FASN protein of xenograft tumour of untreated (4C) and G28UCM-treated non-responding (4T) and responding (12T) group. D. G28UCM treatment does not induce weight loss. The body weight of each mouse was measured before and weekly after treatment with G28UCM (40 mg/Kg/day for 45 days) or vehicle control. Data are expressed as percentage of initial body weight and represent mean values ± SE for each experimental group.

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