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. 2017 Apr 13;8(31):50747–50760. doi: 10.18632/oncotarget.17096

Figure 3. Role of ATM/Chk2/p53 in CUR mediated G2/M cell cycle arrest.

Figure 3

HEp-2 cells were treated with or without CUR for 24 h. Cells were collected and analysed for cell cycle distribution by flow cytometry. (A–D) CUR increased the proportion of cells in G2/M phase and decreased that in the G1 phase, compared with the control group (*P < 0.01). FCM analysis showed CUR arrested HEp-2 cell cycling in the G2/M phase. (E) We observed an increased phosphorylation of H2A.X at Ser-139. At the same time, our results show that CUR treatment decreased the expression of DNA polymerase β1. (F) Treatment of HEp-2 cells with CUR increased the phosphorylation of ATM at Ser-1981. On the other hand, substantial phosphorylation of Cdc25C at Ser-216 was observed in HEp-2 cells treated with CUR. Exposure of HEp-2 cells with 10 μM CUR for 24 h significantly reduced the expression of Cyclin B1. (G) CUR causes cell cycle arrest at the G2/M phase. CUR induces DNA damage and activation of ATM, which phosphorylates H2A.X and CHK2 to induce cell cycle arrest at the G2/M phase by Cdc25c inhibition. CUR mediated effects may occur through a molecular mechanism dependent of ATM/Chk2/p53 signal pathway activation and confirmed our data suggesting the potent anticancer activity of CUR. Data were expressed as mean ± SD. **P < 0.01.