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- W4309413032 abstract "Colorectal cancer (CRC) is a type of ordinary malignancy of the gastrointestinal tract. Atractylenolide I (AT-I) has been shown to inhibit the process of CRC. However, the specific mechanism by which AT-I inhibits CRC is not yet well understood.Cell Counting Kit-8 and colony formation assays were conducted to examine cell proliferation. The cell apoptosis was detected by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling (TUNEL). Cell invasion and migration were evaluated by wound-healing and Transwell assay. The angiogenesis capabilities of the cells were examined by tube formation experiments. Western blot was conducted to examine the apoptosis and angiogenesis-associated proteins, pyruvate dehydrogenase kinase 1 (PDK1), and Forkhead box protein O1 (FoxO1) expression.We found that AT-I inhibited the proliferative, migratory and invasive abilities of Human colorectal cancer cell line HCT116 cells but stimulated cell death by promoting cell apoptosis via the PDK1/FoxO1 axis. In addition, the upregulation of PDK1 decreased the inhibitory effect of AT-I on HCT116 angiogenesis, and AT-I increased oxaliplatin sensitivity via the PDK1/FoxO1 axis.Collectively, AT-I inhibited the malignant development of CRC cells and increased oxaliplatin sensitivity by decreasing PDK1 and inhibiting FoxO1 phosphorylation. Thus, AT-I has protective potential and could be a promising agent for CRC treatment." @default.
- W4309413032 created "2022-11-27" @default.
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- W4309413032 date "2022-10-01" @default.
- W4309413032 modified "2023-10-18" @default.
- W4309413032 title "Atractylenolide I inhibited the development of malignant colorectal cancer cells and enhanced oxaliplatin sensitivity through the PDK1-FoxO1 axis" @default.
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- W4309413032 doi "https://doi.org/10.21037/jgo-22-910" @default.
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