Deletion of p120-catenin results in a tumor microenvironment with inflammation and cancer that establishes it as a tumor suppressor gene.

Stairs DB, Bayne LJ, Rhoades B, Vega ME, Waldron TJ, Kalabis J, Klein-Szanto A, Lee JS, Katz JP, Diehl JA, Reynolds AB, Vonderheide RH, Rustgi AK
Cancer Cell. 2011 19 (4): 470-83

PMID: 21481789 · PMCID: PMC3077713 · DOI:10.1016/j.ccr.2011.02.007

p120-catenin (p120ctn) interacts with E-cadherin, but to our knowledge, no formal proof that p120ctn functions as a bona fide tumor suppressor gene has emerged to date. We report herein that p120ctn loss leads to tumor development in mice. We have generated a conditional knockout model of p120ctn whereby mice develop preneoplastic and neoplastic lesions in the oral cavity, esophagus, and squamous forestomach. Tumor-derived cells secrete granulocyte macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), monocyte chemotactic protein-1 (MCP-1), and tumor necrosis factor-α (TNFα). The tumors contain significant desmoplasia and immune cell infiltration. Immature myeloid cells comprise a significant percentage of the immune cells present and likely participate in fostering a favorable tumor microenvironment, including the activation of fibroblasts.

Copyright © 2011 Elsevier Inc. All rights reserved.

MeSH Terms (16)

Animals Cadherins Carcinoma, Squamous Cell Catenins Cell Differentiation Cell Line, Tumor Cell Proliferation Esophageal Neoplasms Fibroblasts Genes, Tumor Suppressor Humans Inflammation Mice Mouth Neoplasms Myeloid Cells NF-kappa B

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