Open Access

Effect of galectin-3 on the behavior of Eca‑109 human esophageal cancer cells

  • Authors:
    • Ning Liang
    • Xiaoming Song
    • Jian Xie
    • Deguo Xu
    • Fengjun Liu
    • Xinshuang  Yu
    • Yuan Tian
    • Zhen Liu
    • Lili Qiao
    • Jiandong Zhang
  • View Affiliations

  • Published online on: November 5, 2014     https://doi.org/10.3892/mmr.2014.2873
  • Pages: 896-902
  • Copyright: © Liang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Galectin-3, a β-galactoside-binding lectin, is a cell adhesion molecule involved in the regulation of tumor progression. However, the importance of galectin-3 in Eca-109 human esophageal cancer cells has not yet been elucidated. In the present study, a lentiviral vector was designed for overexpression of galectin-3 in Eca-109 cells following plasmid‑mediated transfection (Eca-109/Gal-3 cells). A negative lentiviral vector was introduced into Eca-109 cells as a control (Eca‑109/Neo cells). Western blot and reverse transcription-polymerase chain reaction analyses were used to measure the expression levels of galectin-3 protein and mRNA. The proliferation of Eca-109 cells was measured by a cell counting kit-8 assay. Eca-109 cell apoptosis was determined by Annexin V/7-amino-actinomycin double‑staining. The migration and invasion capacity of Eca-109 cells was determined by a Transwell assay. A total of >98% Eca-109 cells were transfected with the lentiviral vector harboring galectin-3, and galectin-3 expression was detected in Eca-109 cells, Eca-109/Gal-3 cells and Eca-109/Neo cells. Compared with non‑transfected and negative control Eca-109 cells, proliferation was increased significantly in the Eca-109/Gal-3 cells (P<0.05). Galectin-3 also significantly reduced Eca-109 cell apoptosis, compared with the two control groups (P=0.007 and P=0.04, respectively). Transwell migration and invasion assays revealed that significantly greater numbers of Eca-109/Gal-3 cells crossed the artificial basement membrane (55.4±3.9) compared with either the non-transfected or negative control Eca-109 cells (30.6±1.5 and 29±2.6 respectively, P<0.05). In conclusion, galectin-3 expression was significantly increased in transfected Eca-109 esophageal cancer cells, resulting in enhanced proliferation, migration and invasion, as well as reduced apoptosis. These data indicate that galectin-3 may be a potential molecular target in the treatment of esophageal cancer.
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February-2015
Volume 11 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Liang N, Song X, Xie J, Xu D, Liu F, Yu X, Tian Y, Liu Z, Qiao L, Zhang J, Zhang J, et al: Effect of galectin-3 on the behavior of Eca‑109 human esophageal cancer cells. Mol Med Rep 11: 896-902, 2015.
APA
Liang, N., Song, X., Xie, J., Xu, D., Liu, F., Yu, X. ... Zhang, J. (2015). Effect of galectin-3 on the behavior of Eca‑109 human esophageal cancer cells. Molecular Medicine Reports, 11, 896-902. https://doi.org/10.3892/mmr.2014.2873
MLA
Liang, N., Song, X., Xie, J., Xu, D., Liu, F., Yu, X., Tian, Y., Liu, Z., Qiao, L., Zhang, J."Effect of galectin-3 on the behavior of Eca‑109 human esophageal cancer cells". Molecular Medicine Reports 11.2 (2015): 896-902.
Chicago
Liang, N., Song, X., Xie, J., Xu, D., Liu, F., Yu, X., Tian, Y., Liu, Z., Qiao, L., Zhang, J."Effect of galectin-3 on the behavior of Eca‑109 human esophageal cancer cells". Molecular Medicine Reports 11, no. 2 (2015): 896-902. https://doi.org/10.3892/mmr.2014.2873