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

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.

• Authors: Dong Zhang, Zheng-gang Chen, Shao-hua Liu, Zuo-qing Dong, Martin Dalin, Shi-san Bao, Ying-wei Hu, Feng-cai Wei
• Journal: Acta pharmacologica Sinica (Acta Pharmacol Sin) Vol. 34 Issue 1 Pg. 176-84 (Jan 2013) ISSN: 1745-7254 [Electronic] United States
• PMID: 23103626 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

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

Topics

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