상세 정보

underline
Metadata Downloads : dc(xml) or Excel
Cited 0 time in scopus ci

Title 

The cell adhesion molecule L1 promotes gallbladder carcinoma progression in vitro and in vivo

 

담낭암 진행에서 L1CAM 기능 규명

Authors 

Juyeon JungYeon Sung SonH ParkSeong Kook JeonJ W LeeS Y ChoiJ M KimY G KwonH J HongJeong Ki Min

Publisher 

Spandidos Publications

Issue Date 

2011

Citation 

Oncology Reports, vol. 25, no. 4, pp. 945-952

Keywords 

Gallbladder carcinomaL1 cell adhesion moleculeTherapeutic targetTumor progression

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.

ISSN 

1021-335X

Link 

http://dx.doi.org/10.3892/or.2011.1181

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


There are no files associated with this item.
qrcode

FusionCharts.
DSpace Software Coptright(c) 2010 MIT and Hewleft-Packard  /  KRIBB-REPOSITORY ( Email:jakim@kribb.re.kr)