Fig 1: Compound 38a significantly inhibits DSB repair and ATR-CHK1 signalling axis. (A) Representative images of immune-fluorescence staining of γH2AX foci in MDA-MB-231 cells treated with compounds as indicated for 24 h. Scale bar = 100 μm; (B) Western blotting of ATR/p-ATR, CHK1/p-CHK1, p53/p-p53, p21 and γH2AX in MDA-MB-231 cells exposed to different compounds as indicated for 48 h; (C) Statistical analysis of ATR/p-ATR, γH2AX, p-CHK1, p-p53 and p21 protein levels; (D) Mechanism of action of 38a in the treatment of TNBC. The data are shown as the mean ± SD of three independent experiments. NS: no significance. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.