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

Liang N, Song X, Xie J, Xu D, Liu F, Yu X, Tian Y, Liu Z, Qiao L, Zhang J - Mol Med Rep (2014)

Bottom Line: 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).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.

View Article: PubMed Central - PubMed

Affiliation: Division of Oncology, Department of Graduate, Weifang Medical College, Jinan, Shandong 261053, P.R. China.

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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Effect of galectin-3 overexpression on the proliferation of Eca-109 human esophageal cancer cells was determined by a cell counting kit-8 assay. After (A) 12, (B) 24, (C) 48 and (D) 72 h culture, the in vitro growth of the Eca-109/Gal-3 group was significantly increased compared with that of either the Eca-109 or the Eca-109/Neo group (P<0.05). However, no significant differences were identified between the Eca-109 and Eca-109/Neo groups (P>0.05). (E) Growth curves of Eca-109 cells in the three groups.
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f2-mmr-11-02-0896: Effect of galectin-3 overexpression on the proliferation of Eca-109 human esophageal cancer cells was determined by a cell counting kit-8 assay. After (A) 12, (B) 24, (C) 48 and (D) 72 h culture, the in vitro growth of the Eca-109/Gal-3 group was significantly increased compared with that of either the Eca-109 or the Eca-109/Neo group (P<0.05). However, no significant differences were identified between the Eca-109 and Eca-109/Neo groups (P>0.05). (E) Growth curves of Eca-109 cells in the three groups.

Mentions: The effect of galectin-3 overexpression on the proliferation of Eca-109 cancer cells was determined by the CCK-8 assay. Subsequent to culture for 12, 24, 48 and 72 h, the in vitro growth of the Eca-109/Gal-3 group was significantly higher than that of either the Eca-109 or Eca-109/Neo groups at all time points (P<0.05). No significant differences were detected between the Eca-109 and Eca-109/Neo groups at time point (12 h, P=0.563; 24 h, P=0.917; 48 h, P=0.955; 72 h, P=0.495; Fig. 2).


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

Liang N, Song X, Xie J, Xu D, Liu F, Yu X, Tian Y, Liu Z, Qiao L, Zhang J - Mol Med Rep (2014)

Effect of galectin-3 overexpression on the proliferation of Eca-109 human esophageal cancer cells was determined by a cell counting kit-8 assay. After (A) 12, (B) 24, (C) 48 and (D) 72 h culture, the in vitro growth of the Eca-109/Gal-3 group was significantly increased compared with that of either the Eca-109 or the Eca-109/Neo group (P<0.05). However, no significant differences were identified between the Eca-109 and Eca-109/Neo groups (P>0.05). (E) Growth curves of Eca-109 cells in the three groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4262483&req=5

f2-mmr-11-02-0896: Effect of galectin-3 overexpression on the proliferation of Eca-109 human esophageal cancer cells was determined by a cell counting kit-8 assay. After (A) 12, (B) 24, (C) 48 and (D) 72 h culture, the in vitro growth of the Eca-109/Gal-3 group was significantly increased compared with that of either the Eca-109 or the Eca-109/Neo group (P<0.05). However, no significant differences were identified between the Eca-109 and Eca-109/Neo groups (P>0.05). (E) Growth curves of Eca-109 cells in the three groups.
Mentions: The effect of galectin-3 overexpression on the proliferation of Eca-109 cancer cells was determined by the CCK-8 assay. Subsequent to culture for 12, 24, 48 and 72 h, the in vitro growth of the Eca-109/Gal-3 group was significantly higher than that of either the Eca-109 or Eca-109/Neo groups at all time points (P<0.05). No significant differences were detected between the Eca-109 and Eca-109/Neo groups at time point (12 h, P=0.563; 24 h, P=0.917; 48 h, P=0.955; 72 h, P=0.495; Fig. 2).

Bottom Line: 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).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.

View Article: PubMed Central - PubMed

Affiliation: Division of Oncology, Department of Graduate, Weifang Medical College, Jinan, Shandong 261053, P.R. China.

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.

Show MeSH
Related in: MedlinePlus