Fig. 2: Depletion of endogenous PD-L1 enhances radiosensitivity by retardation of DSB repair. | Nature Communications

Fig. 2: Depletion of endogenous PD-L1 enhances radiosensitivity by retardation of DSB repair.

From: PD-L1 deglycosylation promotes its nuclear translocation and accelerates DNA double-strand-break repair in cancer

Fig. 2

a Endogenous PD-L1 was knocked out from H460 cells using the CRISPR/Cas9 system. PD-L1 was rescued by transfection with exogenous WT PD-L1. PD-L1 expression levels were analyzed by western blot. b, c H460 parental, H460 PD-L1 knockout cells and H460 PD-L1 knockout cells expressing exogenous WT PD-L1 were treated with increasing doses of IR, followed by colony formation analysis. Error bars represent ± s.d., n = 3 per group. ***P < 0.001, ****P < 0.0001, by two-tailed t test. d Endogenous PD-L1 was knocked out from H358 cells. PD-L1 was rescued by transfection with exogenous WT PD-L1. PD-L1 expression levels were analyzed by western blot. e, f H358 parental, H358 PD-L1 knockout cells and H358 PD-L1 knockout cells expressing exogenous WT PD-L1 were treated with increasing doses of IR, followed by colony formation analysis. Error bars represent ± s.d., n = 3 per group. ***P < 0.001, by two-tailed t test. g, h H460 parental and PD-L1 knockout H460 cells were treated with 4 Gy of IR at 2 Gy/min dose rate, followed by immunofluorescence analysis of γH2AX foci and DAPI at various time points. Foci ≥5/cell were counted as foci-positive cells. Error bars represent ± s.d., n = 3 per group. ***P < 0.001, by two-tailed t test. Source data are provided as a Source Data file.

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