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. 2017 Mar 8;13(5):3032–3038. doi: 10.3892/ol.2017.5830

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Copyright: © Gu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — (A) G0/G1-phase rate of cells treated with 166.67, 333.33 and 666.67 pM for 48 and 72 h. **P<0.01, compared with the control group between different concentrations. *P<0.05, **P<0.01, compared between different timepoints within the same concentration. (B) S-phase rate of cells treated with 166.67, 333.33 and 666.67 pM for 48 and 72 h. **P<0.01 compared with the control group between difference concentrations. *P<0.05, **P<0.01 compared between different timepoints within the same concentration. (C) G2/M-phase rate of cells treated with 166.67, 333.33 and 666.67 pM for 48 and 72 h. Data is expressed as the mean ± standard deviation of 3 independent experiments performed in triplicate. (D) Cell cycle distribution of cells treated with 666.67 pM MCP30 between 48 and 72 h. These findings indicate that MCP30 induced S-phase arrest. MCP30, Momordica charantia protein.