Isoliquiritigenin inhibits proliferation and induces apoptosis of U87 human glioma cells in vitro

  • Authors:
    • Guo-Sheng Zhou
    • Lai-Jun Song
    • Bo Yang
  • View Affiliations

  • Published online on: December 3, 2012     https://doi.org/10.3892/mmr.2012.1218
  • Pages: 531-536
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Abstract

Isoliquiritigenin (ISL), a member of the flavonoids, has been demonstrated to possess antitumor activity in various cancer cell lines in vitro and in vivo. In this study, we investigated the antitumor effects of ISL on U87 glioma cells in vitro. As determined by MTT assay, ISL inhibited the proliferation of U87 cells in a time-dependent and dose-dependent manner. The results of fluorescence-activated cell sorting (FACS) analysis suggested that ISL induced the apoptosis of the U87 cells and blocked cell cycle progression at the S and G2/M phases. Moreover, it was identified that ISL induced the apoptosis of the U87 cells in a caspase-dependent manner. Although treatment with the pan-caspase inhibitor Z-VAD-FMK efficiently blocked the ISL-induced caspase activation, it did not eliminate the ISL-induced cell death. Further examination using western blot analysis revealed that ISL upregulated p21/WAF1 and p27. These results indicate that cell cycle arrest and the caspase-mediated apoptosis pathway may participate in the antiproliferative activity of ISL in U87 cells by regulating the expression of specific molecules.

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APA
Zhou, G., Song, L., & Yang, B. (2013). Isoliquiritigenin inhibits proliferation and induces apoptosis of U87 human glioma cells in vitro. Molecular Medicine Reports, 7, 531-536. https://doi.org/10.3892/mmr.2012.1218
MLA
Zhou, G., Song, L., Yang, B."Isoliquiritigenin inhibits proliferation and induces apoptosis of U87 human glioma cells in vitro". Molecular Medicine Reports 7.2 (2013): 531-536.
Chicago
Zhou, G., Song, L., Yang, B."Isoliquiritigenin inhibits proliferation and induces apoptosis of U87 human glioma cells in vitro". Molecular Medicine Reports 7, no. 2 (2013): 531-536. https://doi.org/10.3892/mmr.2012.1218