Figure 1: ATM expression and activity promotes HER2 tumorigenicity in vitro.
From: ATM kinase sustains HER2 tumorigenicity in breast cancer
(a–c) Anchorage-independent growth of HER2+ (SKBR3), HER2− (MCF7), exogenous HER2+ (MCF7-HER2) breast cancer cell lines treated with ATM kinase inhibitor KU-55933 10 μM (a,c), infected with retrovirus or expressing specific RNA interference for ATM (shATM#1) or a control sequence (shR5, labelled as −), or infected with lentivirus expressing RNA interference for ATM (shATM#3), for HER2 (shHER2) or a control sequence (shGFP, labelled −) (b). Colonies are counted after 10 days and represented as mean±s.d. (n=6 for each condition). The panels on the bottom display representative western blots. (d) ATM interference selectively impairs NeuT-driven transformation in human mammary gland epithelial cells, MCF10A. Cell proliferation assay in MCF10A-pBabe, MCF10A-NeuT and MCF10A-RasV12 cell lines infected with a lentiviral construct expressing ATM shRNA interference sequence or control shRNA interference sequence. Bars display the cell number for each cell line counted 96 h after seeding; this number has been normalized on cell number counted 24 h after seeding. Cell numbers have been counted in triplicate in three independent experiments for each condition. Data are shown as mean+s.d. (*P value for NeuT versus NeuT-shATM=0.03; P values were calculated using two-sided Student t-tests).
