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Fig. 3 | Breast Cancer Research

Fig. 3

From: Epigenetic silencing of TGFBI confers resistance to trastuzumab in human breast cancer

Fig. 3

Impact of TGFBI expression in trastuzumab-resistant cells. a Representative bright-field microscopy images of TGFBI depletion (Scramble, ShTGFBI A, and ShTGFBI B), overexpression (Mock and TGFBI), and mutagenesis (TGFBImut) in SK and SKTR cells. b Expression analysis by qRT-PCR and Western blot showing the in vitro stable depletion of TGFBI in SK cells (left) and overexpression or mutagenesis of TGFBI in SKTR cells (right). Values of qRT-PCR were determined from triplicates and are expressed as the mean ± SEM. c Cell viability determined by MTT assays upon the use of increasing concentrations of trastuzumab (10−6 to 10 μM) for 5 days. (Upper) The TGFBI depletion in SK did not affect cell viability upon trastuzumab treatment. (Middle) The TGFBI overexpression in SKTR cells (TGFBI) give rise to a major sensitivity to trastuzumab at 10 μM. (Bottom) The TGFBI mutagenesis in SKTR cells (TGFBImut) did not affect cell viability after trastuzumab treatment. Results are expressed as percentage of surviving cells after drug treatment (mean ± SEM). One-way ANOVA using a Tukey HSD post hoc test, **p < 0.01; *p < 0.05 indicate levels of statistical significance. d HER family receptors and their downstream proteins related to PI3K/AKT and MAPK/ERK1/2 pathway characterization in TGFBI-depletion SK cells and TGFBI-overexpression SKTR cells. Western blot showing an enhanced of phosphorylation levels of HER1, HER2, and AKT upon overexpression and mutagenesis of TGFBI in SKTR cells. TGFBI depletion did not produce any change in the HER receptors and their related downstream proteins. Results shown are representative of those obtained from 3 independent experiments and β-actin was used as a control

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