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. 2020 Jun 11;22(2):1527–1535. doi: 10.3892/mmr.2020.11224

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Copyright: © Cao 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 2. — TBMS1 induces the G2/M phase arrest of glioma cells by regulating p21/CDK1/cyclin B1 signaling pathway. U251 and HA cells were incubated with 20, 30 or 40 µg/ml of TBMS1 for 24 h. (A) The DNA synthesis ability was detected via BrdU incorporation. (B) Representative profiles and percentage of cell cycle distribution was determined via flow cytometry. (C) The expression levels and quantitative values of p21, CDK1 and cyclin B1 were monitored by western blot analysis. *P<0.05, **P<0.01 and ***P<0.001 vs. TBMS1 (0 µg/ml). TBMS1, tubeimoside-1; CDK1, cyclin-dependent kinase 1.