AI Article Synopsis
- Mollugin shows strong anti-tumor effects, particularly against HepG2 liver cancer cells, both in laboratory tests (in vitro) and in mice models (in vivo).
- The compound causes cell cycle arrest in the S phase, increases reactive oxygen species (ROS) levels, and leads to DNA damage, indicated by the expression of p-H2AX.
- The findings suggest that the anti-tumor activity of mollugin is linked to its ability to induce DNA damage and disrupt normal cell cycle progression, potentially mitigated by the antioxidant glutathione.
Article Abstract
Mollugin has been proven to have anti-tumor activity. However, its potential anti-tumor mechanism remains to be fully elaborated. Herein, we investigated the growth inhibition of HepG2 cells, as well as the anti-tumor effect of mollugin and its molecular mechanism on H22-tumor bearing mice. In vitro, mollugin was shown to have a strong inhibitory effect on HepG2 cells in a concentration-dependent manner. Mollugin induced S-phase arrest of HepG2 cells, and increased intracellular reactive oxygen species (ROS) levels. Comet assay demonstrated that mollugin induced DNA damage in HepG2 cells, as well as an increase in the expression of p-H2AX. In addition, mollugin induced changes in cyclin A2 and CDK2. However, the addition of antioxidant glutathione (GSH) was able to reverse the effect of mollugin. In vivo, mollugin significantly inhibited tumor growth and reduced the tendency of tumor volume growth in mice. The tumor cell density was found to be decreased in the administration group, and the content of ROS in the tumor tissue significantly increased. The expression of p-H2AX, cyclin A2 and CDK2 were consistent with in vitro results. Mollugin demonstrated anti-hepatocellular carcinoma activity in vitro and in vivo, and its anti-hepatocellular carcinoma activity was found to be related to DNA damage and cell cycle arrest induced by excessive ROS production in cells.
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| http://dx.doi.org/10.1016/j.cbi.2022.109805 | DOI Listing |
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