Journal
JOURNAL OF ETHNOPHARMACOLOGY
Volume 269, Issue -, Pages -Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2020.113705
Keywords
Hard antler extraction; Breast cancer; Invasion; Epithelial-mesenchymal transition; Traditional Chinese medicine; Nuclear factor-kappa B
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Funding
- National Youth Natural Science Foundation Project [30300336]
- Jilin Provincial Science and Technology Directorate Development Plan Item [20190701041GH]
- Province Health Special Project of Jilin Provincial Finance Department [2018SCZWSZX-035]
- Project B of Bethune Program of Jilin University [2012217]
- Special project of health talents in Jilin Province [JLSWSRCZX2020-0042]
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The research indicates that HAE can effectively inhibit self-renewal of stem-like cells, wound healing, and metastasis in breast cancer cells by targeting the NF-kappa B signaling pathway.
Ethnopharmacological relevance: Hard antler extract (HAE) is a traditional Chinese medicine and has potent antitumor, antioxidative, anti-inflammatory, and immunomodulatory activities. Previous studies have demonstrated that HAE can inhibit human prostate cancer metastasis and murine breast cancer proliferation. However, the effect of HAE on human breast cancer cells has not been clarified. Aim of the study: To investigate the effects and underlying mechanism of HAE on self-renewal of stem-like cells and spontaneous and transforming growth factor (TGF)-81-enhanced wound healing, invasion and epithelial-mesenchymal transition (EMT) in breast cancer cells. Methods: HAE was prepared from sika deer by sequential enzymatic digestions and the active compounds were determined by HPLC. The effects of HAE on the viability, mammosphere formation, wound healing and invasion of MDA-MB-231 and SK-BR3 cells were determined. The impact of HAE treatment on spontaneous and TGF-81promoted EMT and the nuclear factor (NF)-kappa B signaling in breast cancer cells was examined by quantitative RTPCR and western blotting. Results: Treatment with HAE at varying concentrations did not change the viability of breast cancer cells. However, HAE at 0.25 or 0.5 mg/mL significantly reduced the number and size of formed mammospheres, and inhibited spontaneous and TGF-81-enhanced wound healing, invasion and EMT in MDA-MB-231 and SK-BR3 cells in a dose-dependent manner. TGF-81 treatment significantly decreased I kappa B alpha expression and increased NF-kappa Bp65 phosphorylation in breast cancer cells, indicating that TGF-81 enhanced NF-kappa B signaling. In contrast, HAE treatment attenuated the spontaneous and TGF-81-enhanced NF-kappa B signaling in breast cancer cells. Conclusion: Our data indicated that HAE inhibited the self-renewal of stem-like cells and spontaneous and TGF81-enhanced wound healing, invasion and EMT in breast cancer cells by attenuating the NF-kappa B signaling in vitro.
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