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Fig. 6 | Breast Cancer Research

Fig. 6

From: Combinatorial targeting of a chromatin complex comprising Dot1L, menin and the tyrosine kinase BAZ1B reveals a new therapeutic vulnerability of endocrine therapy-resistant breast cancer

Fig. 6

Effect of BAZ1B silencing in MCF-7 BC cells. MCF-7 cell proliferation rate A and Caspase 3/7 activity assay B performed following BAZ1B silencing or treatment with fulvestrant (ICI; 100 nM). C ERα trans-activating activity assessed in MCF-7 cells stably expressing the ERE-Luc reporter gene following BAZ1B silencing or treatment with ICI (100 nM). All data are analyzed respect to the scramble (Silencer Select Negative Control: CTRL). Data are presented as the mean ± SD of determinations from a representative experiment performed in six independent replicates after 72 h of silencing. D RT-qPCR (upper panel) analysis of ESR1 (ERα) and TFF1 mRNA levels following BAZ1B silencing. RT-qPCR results are shown as mean ± SD of triplicate determinations from a representative experiment after 72 h of silencing. Western blot (left lower panel) and relative densitometry (right lower panel) showing BAZ1B and ERα protein level following BAZ1B silencing or treatment with ICI (100 nM). β-actin (ACTB) was used as control. Images were processed with ImageJ software (https://imagej.net) for densitometry readings. E) Cell proliferation rate (left) and western blot analysis (right) comparing MCF-7 and MCF-7-flag cells following BAZ1B silencing. For MTT assay, all data are analyzed respect to the scramble (Silencer Select Negative Control: CTRL). Data are presented as the mean ± SD of determinations from a representative experiment performed in six independent replicates after 72 h of silencing. Western blot analysis showing BAZ1B and ERα protein level following BAZ1B silencing. β-actin (ACTB) was used as control. Asterisks indicate statistically significant differences (*p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.005) to CTRL

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