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. 2021 Feb 3;118(6):e2015654118. doi: 10.1073/pnas.2015654118

Fig. 1.

Fig. 1.

Genome-wide RNAi screen identifies ATR pathway as a synergistic target to overcome chemoresistance in SLFN11-deficient cells. (A) Schematic overview of genome-wide RNAi screen workflow in DU145 WT and SLFN11 KO cells. (B and C) Ranked distribution plots of z-scores obtained from cell viability (CPT-treated/untreated) in SLFN11-KO (B) and -WT (C) cells (Dataset S1). Black dots: Individual siRNA targeted genes. Red dots: Hit genes selected for further validation. (D) Protein interaction network with RNAi screen hits in SLFN11-KO cells generated by STRING analysis. Line thickness represents the strength of data confidence. (E) GO analysis of molecular network in SLFN11-KO cells. (FH) Validation of chemosensitivity in SLFN11-WT and KO cells. Cells were transfected with three siRNAs targeting ATR, CHK1, and BRCA2 and then treated with the indicated concentrations of CPT for 72 h. Cell viability was analyzed by CellTiter-Glo (Promega). Error bars represent SD (n = 3).