Fig 2: Breast cancer specific survival among ER-positive patients based on Tamoxifen treatment. (A) Breast cancer specific survival among ER-positive patients with medium/low level of RECQL protein based on Tamoxifen treatment. (B) Breast cancer specific survival among ER-positive patients with high level of RECQL protein based on Tamoxifen treatment.

Fig 3: Cells from a patient with RECON syndrome display a reduced efficiency of replication in the presence of TOP1/2 inhibitors.(A) LCLs and (B) complemented RECQL1-P1-1 patient fibroblasts were sequentially labeled with CldU (red) and IdU (green) as shown. Stalled forks (red-only tracks) were quantified. The mean of 4 independent experiments is shown. A minimum of 200 forks were counted per condition. #P < 0.05 and ##P < 0.01, by 1-way ANOVA with Tukey’s multiple-comparison test. (C) LCLs and (D) complemented fibroblasts were sequentially labeled with CldU and IdU (with or without 50 nM CPT or ETOP) as shown. The length of the CldU and IdU tracks of dual-labeled DNA fibers (>150 per condition) was measured, and the ratio of IdU/CldU track length was calculated, which represents the efficiency of replication in the presence or absence of CPT or ETOP. The median of 3 independent experiments is shown (red line). ###P < 0.001, by Kruskal-Wallis test with Dunn’s multiple comparison.

Fig 4: RECQL prevents DNA double-strand break formation in human cancer cells.(A) RECQL expression levels of different cancer cell lines transfected with control and RECQL siRNAs measured by qRT-PCR. Error bars denote the SD of two independent experiments. (B) Tail moments of different cancer cell lines transfected with control and RECQL siRNAs. Mean of each condition is indicated by the red line and number. P-values are indicated above each cell line. (C, D) Tail moments of VU120T (C) and OCUB-M (D) cancer cells transfected with control and RECQL siRNAs and treated with and without 12.5 μM (C) and 6.25 μM (D) Mirin, respectively. SDs are plotted in black and red bars denote the mean. For (B, C, D), more than 50 cells for each condition were analyzed using CASP software. SDs are plotted in black and red bars denote the mean. Significance is indicated (one-way ANOVA nonparametric Kruskal–Wallis test).

Fig 5: Cells from a patient with RECON syndrome exhibit reduced replication fork restart and increased replication fork degradation following exposure to HU.(A). Complemented RECQL1-P1-1 patient fibroblasts were labeled with CldU and IdU following exposure to 2 mM HU as shown. Stalled forks were quantified. The mean of 3 independent experiments is shown. A minimum of 200 forks were counted per condition. ##P < 0.001, by 1-way ANOVA with Tukey’s multiple-comparison test. (B) Cells from A were labeled with CldU and IdU as shown in A. The IdU/CldU ratio was calculated for a minimum of 100 forks per condition from 3 independent repeats. The IdU/CldU ratio represents the efficiency of replication in the absence HU and the efficiency of replication fork restart following removal of HU. (C) Cells from A were labeled with CldU and IdU and then exposed to 4 mM HU as shown. The IdU/CldU ratio was calculated for a minimum of 100 forks per condition from 3 independent experiments. An IdU/CldU ratio of less than 1 indicates replication fork degradation. ###P < 0.0001, by Kruskal-Wallis test with Dunn’s multiple comparison (B and C).