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LAMC2 enhances the metastatic potential of lung adenocarcinoma

 Y W Moon  ;  G Rao  ;  J J Kim  ;  H-S Shim  ;  K-S Park  ;  S S An  ;  B Kim  ;  P S Steeg  ;  S Sarfaraz  ;  L Changwoo Lee  ;  Donna Voeller  ;  E Y Choi  ;  Ji Luo  ;  D Palmieri  ;  H C Chung  ;  J-H Kim  ;  Y Wang  ;  G Giaccone 
 Cell Death and Differentiation, Vol.22(8) : 1341-1352, 2015 
Journal Title
 Cell Death and Differentiation 
Issue Date
Adenocarcinoma/metabolism* ; Adenocarcinoma/pathology* ; Animals ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Movement/physiology ; Epithelial-Mesenchymal Transition/genetics ; Epithelial-Mesenchymal Transition/physiology ; Female ; Humans ; Laminin/genetics ; Laminin/metabolism* ; Lung Neoplasms/metabolism* ; Lung Neoplasms/pathology* ; Mice
Lung cancer is the number one cancer killer, and metastasis is the main cause of high mortality in lung cancer patients. However, mechanisms underlying the development of lung cancer metastasis remain unknown. Using genome-wide transcriptional analysis in an experimental metastasis model, we identified laminin γ2 (LAMC2), an epithelial basement membrane protein, to be significantly upregulated in lung adenocarcinoma metastatic cells. Elevated LAMC2 increased traction force, migration, and invasion of lung adenocarcinoma cells accompanied by the induction of epithelial-mesenchymal transition (EMT). LAMC2 knockdown decreased traction force, migration, and invasion accompanied by EMT reduction in vitro, and attenuated metastasis in mice. LAMC2 promoted migration and invasion via EMT that was integrin β1- and ZEB1-dependent. High LAMC2 was significantly correlated with the mesenchymal marker vimentin expression in lung adenocarcinomas, and with higher risk of recurrence or death in patients with lung adenocarcinoma. We suggest that LAMC2 promotes metastasis in lung adenocarcinoma via EMT and may be a potential therapeutic target.
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Joo Hang(김주항)
Moon, Yong Wha(문용화)
Shim, Hyo Sup(심효섭) ORCID logo https://orcid.org/0000-0002-5718-3624
Chung, Hyun Cheol(정현철) ORCID logo https://orcid.org/0000-0002-0920-9471
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