Fig. 1: Loss of ERCC6L2 induces ATMi resistance in cancer cells.
From: Phase separation of ERCC6L2–CtIP regulates the extent of DNA end resection
a–h, Clonogenic survival assays of U2OS (a and b), HeLa (c and d), DLD-1 (e and f) and HCT116 (g and h) cells after treatment with KU-60019 (a, c, e and g) or KU-55933 (b, d, f and h) in stable clones of ERCC6L2 KO via CRISPR–Cas9. #1 and #2 indicate independent sgRNAs. Colony formation was quantified based on the area covered by colonies. Data are presented as mean ± s.d. (n = 3 biological replicates, two-way ANOVA). i,j, Clonogenic survival assays detecting the impact of ERCC6L2 rescue after treatment with ATMi (KU-60019) in ERCC6L2-KO U2OS (i) and DLD-1 (j) cells. Colony formation was quantified based on the area covered by colonies. Data are presented as mean ± s.d. (n = 3 biological replicates, two-way ANOVA). k–m, Xenograft assay of ERCC6L2 in DLD-1 cells (n = 7 per group). Nude mice were injected subcutaneously with control (Ctrl) or ERCC6L2-KO DLD-1 cells, and randomly assigned to treatment with DMSO or ATMi (KU-55933, 10 mg kg−1). Tumour images (k), tumour volume (l) and tumour weight (m) are shown. Data are presented as mean ± s.d. (n = 7 biologically independent mice, two-way ANOVA or two-tailed Student’s t-test).
