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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: APE1 promotes non-homologous end joining by initiating DNA double-strand break formation and decreasing ubiquitination of artemis following oxidative genotoxic stress

Fig. 5

The endonuclease activity of APE1 is required for cell survival after IR treatment. a–b HeLa and SiHa cell lines were plated and treated with IR at the indicated doses. Colony formation assays were performed to compare sensitivities of the NC and shAPE1 cells. c–f HeLa and SiHa cells were pre-incubated with Inhibitor III c, e or E3330 d, f at the indicated doses for 6 h prior to 3 Gy IR treatment. Colony formation assays were then performed to analysis of survival ability. (g-i) NC and shAPE1 cells of HeLa and SiHa cell line were treated with IR, and allowed to recover for 96 h, followed by DAPI staining. The representative graph (HeLa) treated by IR was shown in g. h–i Quantitative analysis of proportion of the number of cells with MNs. j The APE1 expression was evaluated by IHC in tumor tissues and paired peri-tumor tissues of 16 cervix cancer samples. The representative images were shown (left) and the bar graph showing the percentage of each score level of APE1 in peri-tumor and tumor tissue, respectively (right). k–l The tissue expression of APE1 were evaluated by IHC in 46 cervix cancer patients receiving radical chemo-radiotherapy. Protein levels were scored for four categories: score-, score + , score +  + , and score +  +  + . The representative images were shown k. Kaplan–Meier plot showing different overall survival of cervical cancer patients according to APE1 expression l. The data were presented as the mean ± SEM from three independent experiments. The p-values were determined using an unpaired Student’s t-test (**p < 0.01, *p < 0.05)

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