Journal of International Oncology ›› 2014, Vol. 41 ›› Issue (5): 375-379.doi: 10.3760/cma.j.issn.1673-422X.2014.05.017

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Effect of galectin3 on proliferation and migration of esophageal cancer Eca109 cells

Liang Ning, Xie Jian, Qiao Lili, Zhang Jiandong   

  1. Graduate School, Weifang Medical College, Weifang 261061, China
  • Received:2013-12-05 Revised:2014-02-25 Online:2014-05-08 Published:2014-04-28
  • Contact: Zhang Jiandong E-mail:zhangjd165@sina.com

Abstract: Objective To investigate galectin3 on proliferation and migration of esophageal cancer Eca109 cells. Methods A lentiviral vector for overexpression of RNA targeting galectin3 was designed to transfect Eca109 cancer cells following plasmidmediated transfection manual (Eca109/Gal3 cells). Inverted fluorescence microscope was used to observe the expression of EGFP. The proliferation of Eca109 cells was measured by cell counting Kit8 assay. Eca109 cells apoptosis was determined by AnnexinV/7AAD doublestaining. The migration capacity of Eca109 cells was determined in transwell assays. Western blot analysis was used to measure the expression of galectin3 protein. ResultsGalectin3 expression was detected in Eca109 cells, with the Galectin3 expression in Eca109/Gal3 cells much more than nontransfected cells (t=14.33, P<0.05; t=10.28, P=0.037). Compared with nontransfected Eca109 cells, proliferation increased significantly in Eca109/Gal3 cells (t=-17.277, P<0.05; t=-13.4, P<0.05). Galectin3 evidently decreased in Eca109 cell apoptosis (t=3.053, P<0.05; t=5.446, P<0.05). Transwell migration assay showed that a greater number of Eca109/Gal3 cells crossed the artificial basement membrane compared with nontransfected Eca109 cells and negative control Eca109 cells (t=3.465, P<0.05; t=3.252, P<0.05). Conclusion Galectin3 expression is detected in transfected esophageal cancer Eca109 cells, whose overexpression can result in enhanced proliferation, migration, invasion as well as reduced apoptosis. These data indicate that indepth research of galectin3 may prove to be a potential molecular target for the treatment of esophageal cancer.

Key words: Esophageal neoplasms, Galectin 3, RNA over-expression, Biological function