LAMC2 Increases the Metastatic Potential of Lung Adenocarcinoma

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Mechanisms of lung cancer metastasis remain largely undefined. In a study reported in Cell Death & Differentiation that used genome-wide transcriptional analysis in a metastasis model, Moon and colleagues found that the epithelial basement membrane protein laminin γ2 (LAMC2) was significantly upregulated in lung adenocarcinoma metastatic cells.

Elevated LAMC2 was associated with increased traction force, migration, and invasion of lung adenocarcinoma cells and induction of epithelial-mesenchymal transition. LAMC2 knockdown resulted in decreased traction force, migration, and invasion and reduced epithelial-mesenchymal transition reduction in vitro and reduced metastasis in a mouse model. The migration and invasion mediated by epithelial-mesenchymal transition were integrin β1- and ZEB1-dependent. High LAMC2 levels were significantly associated with expression of the mesenchymal marker vimentin and were significantly associated with a higher risk of tumor recurrence or death in lung cancer patients.

The investigators concluded: “We suggest that LAMC2 promotes metastasis in lung adenocarcinoma via epithelial-mesenchymal transition and may be a potential therapeutic target.” ■

Moon YW, et al. Cell Death Differ. January 16, 2015 (early release online).