Galectin-3 gene silencing inhibits migration and invasion of human tongue cancer cells in vitro via downregulating β-catenin

Acta Pharmacol Sin. 2013 Jan;34(1):176-84. doi: 10.1038/aps.2012.150. Epub 2012 Oct 29.

Abstract

Aim: Galectin-3 (Gal-3) is a member of the carbohydrate-binding protein family that contributes to neoplastic transformation, tumor survival, angiogenesis, and metastasis. The aim of this study is to investigate the role of Gal-3 in human tongue cancer progression.

Methods: Human tongue cancer cell lines (SCC-4 and CAL27) were transfected with a small-interfering RNA against Gal-3 (Gal-3-siRNA). The migration and invasion of the cells were examined using a scratch assay and BD BioCoat Matrigel Invasion Chamber, respectively. The mRNA and protein levels of β-catenin, Akt/pAkt, GSK-3β/pGSK-3β, MMP-9 in the cells were measured using RT-PCR and Western blotting, respectively.

Results: Transient silencing of Gal-3 gene for 48 h significantly suppressed the migration and invasion of both SCC-4 and CAL27 cells. Silencing of Gal-3 gene significantly decreased the protein level of β-catenin, leaving the mRNA level of β-catenin unaffected. Furthermore, silencing Gal-3 gene significantly decreased the levels of phosphorylated Akt and GSK-3β, and suppressed the mRNA and protein levels of MMP-9 in the cells.

Conclusion: Our data suggest that Gal-3 mediates the migration and invasion of tongue cancer cells in vitro via regulating the Wnt/β-catenin signaling pathway and Akt phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Cell Movement
  • Down-Regulation
  • Galectin 3 / genetics*
  • Humans
  • Neoplasm Invasiveness / genetics
  • Neoplasm Invasiveness / pathology
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA Interference*
  • RNA, Messenger / genetics
  • Tongue / metabolism
  • Tongue / pathology*
  • Tongue Neoplasms / genetics
  • Tongue Neoplasms / metabolism
  • Tongue Neoplasms / pathology*
  • Transfection
  • Wnt Signaling Pathway
  • beta Catenin / genetics*
  • beta Catenin / metabolism

Substances

  • Galectin 3
  • RNA, Messenger
  • beta Catenin
  • Proto-Oncogene Proteins c-akt