Clones constitutively expressing wild type L1 (L1), a mutant L1 (mut L1), or empty vector were treated with various concentrations of TGF-β1 or control (A), Receptor tyrosine kinase inhibitors: sunitinib malate (VEGFR2, PDGFRβ and c-KIT inhibitor) (B), EGFR inhibitors- Erlotinib (C) and Gefitinib (D). After 72 h of treatment, proliferation was determined by the MTT assay and normalized to untreated or DMSO (vehicle for receptor tyrosine kinase inhibitors) for each cell type. Data represent the mean plus SEM for individual samples from three independent experiments. (E) Stably transfected cells were serum-starved for 24 h and cell lysates analyzed by immunoblotting for phospho-ERK1/2 (p-Erk1/2), phospho-AKT1 (p-Akt), ERK1/2 or AKT1 (Akt). Data are representative two independent experiments using clones #5 (wild type L1) and #13 (mutant L1).