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acrjourna erogeneous nuclear ribonucleoprotein A2/B1 (hnRNP A2/B1) has been reported to be overexpressed in ancer and in other cancers such as breast, pancreas, and liver. However, a mechanism linking hnRNP A2/ rexpression and progression to cancer has not yet been definitively established. To elucidate this mech, we have silenced hnRNPA2/B1 mRNA in non–small-cell lung cancer cell lines A549, H1703, and H358. cell lines present different levels of expression of epithelial-to-mesenchymal transition (EMT) markers s E-cadherin, fibronectin, and vimentin. Microarray expression analysis was performed to evaluate the of silencing hnRNP A2/B1 in A549 cells. We identified a list of target genes, affected by silencing of hnRNP , that are involved in regulation of migration, proliferation, survival, and apoptosis. Silencing hnRNP A2/ uced formation of cell clusters and increased proliferation. In the anchorage-independent assay, silencing A2/B1 increased colony formation by 794% in A549 and 174% in H1703 compared with a 25% increase in ration, in both cell lines, in a two-dimensional proliferation assay. Silencing hnRNP A2/B1 decreased ion in intermediate cell line A549 and mesenchymal cell line H1703; however, no changes in proliferation bserved in epithelial cell line H358. Silencing hnRNP A2/B1 in A549 and H1703 cells correlated with an se of E-cadherin expression and downregulation of the E-cadherin inhibitors Twist1 and Snai1. These increa data suggest that expression of hnRNP A2/B1 may play a role in EMT, in nonepithelial lung cancer cell lines A549 and H1703, through the regulation of E-cadherin expression. Cancer Res; 70(18); 7137–47. ©2010 AACR.