Abstract
Ixeris dentata (Thunb. Ex Thunb.) Nakai (ID) exhibits various physiological activities, and its related plant derived-products are expected to represent promising cancer therapeutic agents. However, the anticancer effects of ID extract on breast cancer cells classified as estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) are still unknown. In this study, we investigated the anti-cancer effects and analyzed the molecular mechanism of ID extract in T47D, MCF-7 (ER-, PR-positive, HER2-negative), SK-BR-3(ER-, PR-negative, HER2-positive), and MDA-MB-231 (Triple-negative) through in vitro studies. Additionally, we examined its anti-tumor effects through in vivo studies. Our findings indicated that ID extract-induced apoptosis was mediated via various survival pathways on four breast cancer cells by identifying the factors including Bcl-2 family, phospho-Akt and phospho-nuclear factor-κB (NF-κB). Based on in vitro findings that induced apoptosis via Akt-NF-κB signaling, we investigated the effects of ID extract on mice bearing MDA-MB-231 cells. The results showed that ID extract significantly decreased MDA-MB-231 tumor volume and weight via inducing apoptosis by suppressing phospho-Akt. Overall, these results indicate that ID extract induces apoptosis through the Akt-NF-κB signaling pathway in MDA-MB-231 breast cancer cells and tumors, and it may serve as a therapeutic agent for triple-negative human breast cancer.
Highlights
Breast cancer is the most common type of cancer to affect women worldwide, accounting for 23% of all cancer diagnoses and 14% of cancer-related deaths [1]
To identify the effect of Ixeris dentata (ID) extract on the survival rate of breast cancer cells, T47D, MCF-7, SK-BR-3, and MDA-MB-231 cells were treated with various concentrations of ID extract (0, 6.25, 12.5, 25, 50, 100, or 200 μg/mL) for 24 h, and the viability of cells was measured as compared with untreated controls using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay
These results suggest that ID extract induces cell death and inhibits cell viability in T47D, MCF-7, SK-BR-3, and MDA-MB-231 cells at concentrations ≥100 μg/mL
Summary
Breast cancer is the most common type of cancer to affect women worldwide, accounting for 23% of all cancer diagnoses and 14% of cancer-related deaths [1]. Various genetic and environmental factors, including family history and a Westernized diet, are regarded as the major risk factors for breast cancer, but the exact cause has not yet been identified [2]. Breast cancer can be categorized according to the expression of hormone receptors, including estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). ER-negative breast cancers, which account for almost 25%–30% of all breast cancers, have a poorer prognosis than that of ER-positive cancers [3,4]. All types of breast cancer have a risk of relapse, and prognosis is poor after breast cancer recurrence [5,6]. An exploration of novel therapeutic agents is needed for the treatment and prevention of breast cancer
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