Abstract
Alpinia officinarum (A. officinarum), a member of the ginger family, is used in traditional medicine to treat stomach ache, cold and swelling. Previous studies have demonstrated an anticancer effect of the A. officinarum extract and its major components in several cancer cell lines. However, the molecular mechanisms underlying the activity of this extract in breast cancer cells have not been fully elucidated to date. The aim of the present study was to investigate the molecular mechanisms underlying the activity of a methanolic extract of A. officinarum, by examining its effects on the proliferation of the breast cancer cell line MCF-7. Notably, the extract inhibited MCF-7 cell proliferation in a dose- and time‑dependent manner. To further elucidate the molecular mechanism, we examined whether the A. officinarum extract affected cell cycle progression in MCF-7 cells. The extract inhibited S-phase cell cycle progression by suppressing the expression levels of S-phase cell cycle regulatory proteins, including E2F1, cyclin‑dependent protein kinase 2 and cyclin A. Additionally, nuclear morphology and flow cytometry with Annexin V/propidium iodide dual staining demonstrated that apoptosis was induced. Western blot analysis using antibodies against apoptosis‑related proteins showed that cell death induced by the extract is mediated via caspase‑ and mitochondrial‑dependent pathways. These findings collectively indicate that the A. officinarum extract exerts an antiproliferative activity in MCF-7 breast cancer cells by inducing S-phase cell cycle arrest and apoptosis.
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