Amorphophalli Rhizoma inhibits breast cancer growth, proliferation, migration, and invasion via the PI3K/AKT pathway
Amorphophalli Rhizoma (APR) is widely used as an adjuvant treatment for advanced and metastatic triple-negative breast cancer (TNBC), but its effects, potential active ingredients, and mechanism of action on estrogen receptor-positive (ER+) and human epidermal growth factor receptor-positive (HER2+)...
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Veröffentlicht in: | Journal of ethnopharmacology 2022-03, Vol.286, p.114926-114926, Article 114926 |
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Zusammenfassung: | Amorphophalli Rhizoma (APR) is widely used as an adjuvant treatment for advanced and metastatic triple-negative breast cancer (TNBC), but its effects, potential active ingredients, and mechanism of action on estrogen receptor-positive (ER+) and human epidermal growth factor receptor-positive (HER2+) breast cancer cells were not reported.
The present study investigated the effects and mechanism of APR on ER+ and HER2+ breast cancer cells.
Rotary evaporation was used to prepare different extracts of APR. Cell activity was assessed using the cell counting kit-8 (CCK-8) method. Wound healing assays were used to assess cell migration, and a cell invasion assay was performed using a Transwell chamber with Matrigel matrix. A xenograft model was used to analyze the inhibitory effects of APR on tumor growth. Bioinformatics analyses were used to explore the potential mechanism of APR in breast cancer. RT–qPCR and Western blotting were performed to reveal the molecular mechanism.
The ethyl acetate extract of APR showed the strongest tumor inhibitory effect on ER+ and HER2+ breast cancer cells compared to petroleum ether or N-butanol extracts. APR inhibited ER+ and HER2+ breast cancer cell growth, proliferation, migration, and invasion via the phosphatidylinositol-3 kinase (PI3K)/AKT pathway.
APR had a significant inhibitory effect on ER+ and HER2+ breast cancer cells via the PI3K/AKT signaling pathway. Therefore, APR may be useful for preventing ER+ and HER2+ breast tumor growth, proliferation, migration, and invasion.
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•APR inhibited cell growth, proliferation, migration, and invasion in ER + breast cancer cells.•APR inhibited cell growth, proliferation, migration, and invasion in HER2+ breast cancer cells.•APR activated the PI3K/AKT signaling pathway.•Different extracts have different cytotoxicity to different types of breast cancer cells.•Different cytotoxicity plays a key role in the accurate treatment of breast cancer. |
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ISSN: | 0378-8741 1872-7573 |
DOI: | 10.1016/j.jep.2021.114926 |