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Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis

  • Authors:
    • Wei Di
    • Lanwei Zhang
    • Huaxi Yi
    • Xue Han
    • Yingchun Zhang
    • Liang Xin
  • View Affiliations / Copyright

    Affiliations: Department of Food Science and Engineering, School of Chemistry and Chemical Engineering, Harbin Institute of Technology, Harbin, Heilongjiang 150090, P.R. China, Functional Dairy and Probiotics Engineering Laboratory, College of Food Science and Engineering, Ocean University of China, Qingdao, Shandong 266003, P.R. China
    Copyright: © Di et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3577-3586
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    Published online on: July 11, 2018
       https://doi.org/10.3892/ol.2018.9129
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Abstract

In the present study, the effects of exopolysaccharides (EPS) from nine Lactobacillus strains with a high degree of bio‑activity on human colon cancer cell line HT‑29 were studied. The extracellular polymeric substances from 4 strains, namely K11, M5, SB27 and X12, displayed desirable anti‑proliferative activity against HT‑29 cells. Crude and acidic EPS were purified from the 4 strains and the inhibitory effects were further investigated. The crude and acidic EPS from these 4 strains exerted anti‑proliferation effects on HT‑29 cells in a dose‑dependent manner but were nontoxic to Vero cells. Treatment with EPS significantly induced G0/G1 cell cycle arrest and apoptosis of HT‑29 cells. Hoechst 33258 staining of acidic EPS‑treated HT‑29 cells revealed different degrees of morphological changes within the nucleus and the formation of apoptotic bodies. Caspase‑3 activity was markedly upregulated in HT‑29 cells following treatment with acidic EPS. In addition, acidic EPS from the SB27 strain demonstrated the most robust inhibitory effect on HT‑29 cells. The results of the present study suggest that as an inducer of apoptosis EPS has the potential to be applied in the treatment of colorectal cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Di W, Zhang L, Yi H, Han X, Zhang Y and Xin L: Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis. Oncol Lett 16: 3577-3586, 2018.
APA
Di, W., Zhang, L., Yi, H., Han, X., Zhang, Y., & Xin, L. (2018). Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis. Oncology Letters, 16, 3577-3586. https://doi.org/10.3892/ol.2018.9129
MLA
Di, W., Zhang, L., Yi, H., Han, X., Zhang, Y., Xin, L."Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis". Oncology Letters 16.3 (2018): 3577-3586.
Chicago
Di, W., Zhang, L., Yi, H., Han, X., Zhang, Y., Xin, L."Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis". Oncology Letters 16, no. 3 (2018): 3577-3586. https://doi.org/10.3892/ol.2018.9129
Copy and paste a formatted citation
x
Spandidos Publications style
Di W, Zhang L, Yi H, Han X, Zhang Y and Xin L: Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis. Oncol Lett 16: 3577-3586, 2018.
APA
Di, W., Zhang, L., Yi, H., Han, X., Zhang, Y., & Xin, L. (2018). Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis. Oncology Letters, 16, 3577-3586. https://doi.org/10.3892/ol.2018.9129
MLA
Di, W., Zhang, L., Yi, H., Han, X., Zhang, Y., Xin, L."Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis". Oncology Letters 16.3 (2018): 3577-3586.
Chicago
Di, W., Zhang, L., Yi, H., Han, X., Zhang, Y., Xin, L."Exopolysaccharides produced by Lactobacillus strains suppress HT‑29 cell growth via induction of G0/G1 cell cycle arrest and apoptosis". Oncology Letters 16, no. 3 (2018): 3577-3586. https://doi.org/10.3892/ol.2018.9129
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