The cell adhesion molecule L1 promotes gallbladder carcinoma progression in vitro and in vivo = 담낭암 진행에서 L1CAM 기능 규명

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Title
The cell adhesion molecule L1 promotes gallbladder carcinoma progression in vitro and in vivo = 담낭암 진행에서 L1CAM 기능 규명
Author(s)
Juyeon Jung; Yeon Sung Son; H Park; Seong Kook Jeon; J W Lee; S Y Choi; J M Kim; Y G Kwon; H J Hong; Jeong Ki Min
Bibliographic Citation
Oncology Reports, vol. 25, no. 4, pp. 945-952
Publication Year
2011
Abstract
Recent studies have demonstrated that the cell adhesion molecule, L1, is expressed in several malignant tumor types and its expression correlates with tumor progression and metastasis. However, the role of L1 in gallbladder carcinoma (GBC) remains unclear. Here, we demonstrate that L1 is expressed in GBC cells and plays an important role in the growth, motility, invasiveness, and adhesiveness of GBC cells. Specific depletion or overexpression of L1 in the GBC cell lines JCRB1033 and SNU-308, respectively, was achieved by lentivirus-mediated transduction and expression of an L1 mRNA-specific short hairpin RNA or full-length human L1. Stable depletion of L1 led to a significant decrease in GBC cell proliferation, migration and invasion, as well as decreased intracellular signaling through AKT and FAK. Overexpression of L1 in GBC cells enhanced these cellular activities. In a GBC xenograft nude mouse model, suppression of L1 markedly reduced tumor growth and increased the survival of tumor-bearing mice whereas L1 overexpression stimulated tumorigenicity. Taken together, these results suggest that L1 plays a crucial role in GBC progression and may be a novel therapeutic target in GBC treatment.
Keyword
Gallbladder carcinomaL1 cell adhesion moleculeTherapeutic targetTumor progression
ISSN
1021-335X
Publisher
Spandidos Publ Ltd
DOI
http://dx.doi.org/10.3892/or.2011.1181
Type
Article
Appears in Collections:
Division of Research on National Challenges > Bionanotechnology Research Center > 1. Journal Articles
Division of Biomedical Research > Biotherapeutics Translational Research Center > 1. Journal Articles
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