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- W4361259097 abstract "<div>Abstract<p>The epithelial–mesenchymal transition (EMT) and its reversal, mesenchymal–epithelial transition (MET), are fundamental processes involved in tumor cell invasion and metastasis. SEMA3F is a secreted semaphorin and tumor suppressor downregulated by TGF-β1 and ZEB1-induced EMT. Here, we report that neuropilin (NRP)-2, the high-affinity receptor for SEMA3F and a coreceptor for certain growth factors, is upregulated during TGF-β1–driven EMT in lung cancer cells. Mechanistically, NRP2 upregulation was TβRI dependent and SMAD independent, occurring mainly at a posttranscriptional level involving increased association of mRNA with polyribosomes. Extracellular signal—regulated kinase (ERK) and AKT inhibition blocked NRP2 upregulation, whereas RNA interference-mediated attenuation of ZEB1 reduced steady-state NRP2 levels. In addition, NRP2 attenuation inhibited TGF-β1–driven morphologic transformation, migration/invasion, ERK activation, growth suppression, and changes in gene expression. In a mouse xenograft model of lung cancer, NRP2 attenuation also inhibited locally invasive features of the tumor and reversed TGF-β1–mediated growth inhibition. In support of these results, human lung cancer specimens with the highest NRP2 expression were predominantly E-cadherin negative. Furthermore, the presence of NRP2 staining strengthened the association of E-cadherin loss with high-grade tumors. Together, our results demonstrate that NRP2 contributes significantly to TGF-β1–induced EMT in lung cancer. <i>Cancer Res; 73(23); 7111–21. ©2013 AACR</i>.</p></div>" @default.
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- W4361259097 date "2023-03-30" @default.
- W4361259097 modified "2023-10-16" @default.
- W4361259097 title "Data from Neuropilin-2 Is Upregulated in Lung Cancer Cells during TGF-β1–Induced Epithelial–Mesenchymal Transition" @default.
- W4361259097 doi "https://doi.org/10.1158/0008-5472.c.6504636.v1" @default.
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