Anti-breast cancer effects of live, heat-killed and cytoplasmic fractions of Enterococcus faecalis and Staphylococcus hominis isolated from human breast milk
- 389 Downloads
Development of tumour that is resistant to chemotherapeutics and synthetic drugs, coupled with their life-threatening side effects and the adverse effects of surgery and hormone therapies, led to increased research on probiotics’ anticancer potentials. The current study investigated the potential of live, heat-killed cells (HKC) and the cytoplasmic fractions (CF) of Enterococcus faecalis and Staphylococcus hominis as anti-breast cancer agents. MCF-7 cell line was treated with 25, 50, 100 and 200 μg/mL each of live, HKC and CF of the bacteria; and cytotoxicity was evaluated for 24, 48 and 72 h using MTT assay. The morphological features of the treated cells were examined by fluorescence microscopy. The stage of cell cycle arrest and apoptosis were quantified by flow cytometry. The bacterial effect on non-malignant breast epithelial cell line, MCF-10A, was assessed using MTT assay for 24, 48 and 72 h. All the three forms of the bacteria caused a significant decrease in MCF-7 (up to 33.29%) cell proliferation in concentration- and time-dependent manner. Morphological features of apoptosis like cell death, cell shrinkage and membrane blebbing were observed. Flow cytometry analyses suggested that about 34.60% of treated MCF-7 was undergoing apoptosis. A strong anti-proliferative activity was efficiently induced through sub-G1 accumulation (up to 83.17%) in treated MCF-7 and decreased number in the G0/G1 phase (74.39%). MCF-10A cells treated with both bacteria showed no significant difference with the untreated (>90% viability). These bacteria can be used as good alternative nutraceutical with promising therapeutic indexes for breast cancer because of their non-cytotoxic effects to normal cells.
KeywordsE. faecalis S. hominis Apoptosis Cytotoxicity Breast cancer
This project was supported by Fundamental Research Grants, Ministry of Higher Education, Malaysia (No. 5524244). We also acknowledge the invaluable assistance of Dr. Yeap Swee Keong of the Institute of BioScience, Universiti Putra Malaysia, Serdang, Malaysia, in the flow cytometry analysis and the data interpretation. We are also thankful to Associate Professor Dr. Noorjahan Banu Mohamed Alitheen, Universiti Putra, Malaysia, for allowing us to use her laboratory for some part of the study.
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflict of interest.
- Cooper GM (2000) The cell: a molecular approach, 2nd edn. Boston University, SunderlandGoogle Scholar
- Di-Francia R, Stefania RS, Valente D, Del Buono A, Pugliese S, Cecere S, Berretta M. (2013) Current strategies to minimize toxicity of oxaliplatin : selection of pharmacogenomic panel tests. Anti-Cancer Drugs. 2:1–11. doi: 10.1097/CAD.0000000000000002
- Liu C-F, Pan T-M (2010) In vitro effects of lactic acid bacteria on cancer cell viability and antioxidant activity. J Food Drug Anal 18(2):77–86Google Scholar
- Liu T, Chen C, Yiin S, Chen C, Cheng J, Shih M, Chern C (2006) Molecular mechanism of cell cycle blockage of hepatoma SK-Hep-1 cells by Epimedin C through suppression of mitogen-activated protein kinase activation and increased expression of CDK inhibitors p21 Cip1 and p27 Kip1. Food Chem Toxicol. 44:227–235. doi: 10.1016/j.fct.2005.07.003
- Subhashini S, Meignanalakshmi S (2013) In vitro studies on adhesion and the effect of cytotoxicity of Bifidobacterium spp. using cell lines. Eur Sci J 9(18):311–326Google Scholar
- Thompson A, Brennan K, Cox A, Gee J, Harcourt D, Harris A, Steel M (2008) Evaluation of the current knowledge limitations in breast cancer research : a gap analysis. Breast Cancer Res. 10(R26):1–25. doi: 10.1186/bcr1983
- Wang L, Wu J, Lu J, Ma R, Sun D, Tang J (2014) Regulation of the cell cycle and PI3K/Akt/mTOR signaling pathway by tanshinone I in human breast cancer cell lines. Mol Med Rep. 1–9. doi: 10.3892/mmr.2014.2819
- WHO (2013) Latest world cancer statistics. International Agency for Research on Cancer, World Health Organization. Lyon/Geneva. Retrieved from http://www.iarc.fr/en/media-centre/pr/2013/pdfs/pr223_E.pdf