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LAMC2 enhances the metastatic potential of lung adenocarcinoma.
Moon, Y W; Rao, G; Kim, J J; Shim, H-S; Park, K-S; An, S S; Kim, B; Steeg, P S; Sarfaraz, S; Changwoo Lee, L; Voeller, Donna; Choi, E Y; Luo, Ji; Palmieri, D; Chung, H C; Kim, J-H; Wang, Y; Giaccone, G.
Afiliación
  • Moon YW; 1] Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA [2] Division of Medical Oncology, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea.
  • Rao G; Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
  • Kim JJ; Department of Bioengineering, Johns Hopkins University, Baltimore, MD, USA.
  • Shim HS; Department of Pathology, Yonsei University College of Medicine, Seoul, South Korea.
  • Park KS; 1] Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA [2] Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
  • An SS; Department of Environmental Health Sciences, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, MD, USA.
  • Kim B; Pathology Branch, National Cancer Institute, National Institutes of Health, MD, USA.
  • Steeg PS; Women's Cancers Section, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
  • Sarfaraz S; Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • Changwoo Lee L; Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • Voeller D; Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • Choi EY; Department of Environmental Health Sciences, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, MD, USA.
  • Luo J; Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
  • Palmieri D; Women's Cancers Section, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
  • Chung HC; Division of Medical Oncology, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea.
  • Kim JH; Division of Medical Oncology, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea.
  • Wang Y; 1] Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA [2] Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
  • Giaccone G; 1] Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA [2] Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Cell Death Differ ; 22(8): 1341-52, 2015 Aug.
Article en En | MEDLINE | ID: mdl-25591736
ABSTRACT
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 ß1- 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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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Adenocarcinoma / Laminina / Neoplasias Pulmonares Límite: Animals / Female / Humans Idioma: En Revista: Cell Death Differ Año: 2015 Tipo del documento: Article País de afiliación: Corea del Sur
Texto completo
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XML
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Adenocarcinoma / Laminina / Neoplasias Pulmonares Límite: Animals / Female / Humans Idioma: En Revista: Cell Death Differ Año: 2015 Tipo del documento: Article País de afiliación: Corea del Sur