Fig. 2: ANKHD1 silencing promoted IR-induced DNA double-strand breaks by inhibiting DNA-damage repair signaling. | Cell Death & Disease

Fig. 2: ANKHD1 silencing promoted IR-induced DNA double-strand breaks by inhibiting DNA-damage repair signaling.

From: The feedback loop of ANKHD1/lncRNA MALAT1/YAP1 strengthens the radioresistance of CRC by activating YAP1/AKT signaling

Fig. 2

A The formation of ROS was detected by flow cytometry in HCT116 and HCT8 cells with or without IR (*P < 0.05, **P < 0.01). B A comet assay was conducted to detect DNA damage at 0, 0.5, and 4 h after 4 Gy IR, and the DNA-damage amount was quantified by measuring the comet-tail lengths (*P < 0.05). C Western blotting was used to detect γH2AX at 0, 0.5, 1, 2, 4, and 12 h post IR. D γH2AX foci were detected by immunofluorescence at 0, 0.5, 1, 2, 4, and 12 h post IR in CHT8 cells, and the γH2AX foci number was counted from more than 100 cells (**P < 0.01). E Flow cytometry was used to detect the distribution of the cell cycle; ANKHD1-silenced cells were arrested in G2/M phase at 12 h after 4 Gy IR (*P < 0.05). F The expression of cyclin B1, CDK1, p53, and p21 was detected by Western blotting at 0 and 12 h post IR in HCT116 and HCT8 cells. G The expression of p-ATM, 53BP1, RAD50, MRE11, NBS1, YAP1, and p-CHK2 was detected by Western blot at 0, 0.5 and 4 h post IR in HCT116 and HCT8 cells. H ANKHD1 silencing increased apoptosis at 48 h post IR in HCT116 cells (*P < 0.05). I ANKHD1 silencing increased the expression of cleaved-caspase 3 at 48 h post IR.

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