| Autor: |
Xu, Haiying, Li, Lanqing, Qu, Linghang, Tu, Jiyuan, Sun, Xiongjie, Liu, Xianqiong, Xu, Kang |
| Zdroj: |
Phytotherapy Research; Mar2023, Vol. 37 Issue 3, p820-833, 14p |
| Abstrakt: |
Atractylenolide‐1 (AT‐1) is a major octanol alkaloid isolated from Atractylodes Rhizoma and is widely used to treat various diseases. However, few reports have addressed the anticancer potential of AT‐1, and the underlying molecular mechanisms of its anticancer effects are unclear. This study aimed to assess the effect of AT‐1 on triple‐negative breast cancer (TNBC) cell proliferation and migration and explore its potential molecular mechanisms. Cell invasion assays confirmed that the number of migrating cells decreased after AT‐1 treatment. Colony formation assays showed that AT‐1 treatment impaired the ability of MDA‐MB‐231 cells to form colonies. AT‐1 inhibited the expression of p‐p38, p‐ERK, and p‐AKT in MDA‐MB‐231 cells, significantly downregulated the proliferation of anti‐apoptosis‐related proteins CDK1, CCND1, and Bcl2, and up‐regulated pro‐apoptotic proteins Bak, caspase 3, and caspase 9. The gas chromatography–mass spectroscopy results showed that AT‐1 downregulated the metabolism‐related genes TPI1 and GPI through the glycolysis/gluconeogenesis pathway and inhibited tumor growth in vivo. AT‐1 affected glycolysis/gluconeogenesis by downregulating the expression of TPI1 and GPI, inhibiting the proliferation, migration, and invasion of (TNBC) MDA‐MB‐231 cells and suppressing tumor growth in vivo. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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