Deletion of p120-Catenin Results in a Tumor Microenvironment with Inflammation and Cancer that Establishes It as a Tumor Suppressor Gene

Douglas B. Stairs, Lauren J. Bayne, Ben Rhoades, Maria E. Vega, Todd J. Waldron, Jiri Kalabis, Andres Klein-Szanto, Ju Seog Lee, Jonathan P. Katz, J. Alan Diehl, Albert B. Reynolds, Robert H. Vonderheide, Anil K. Rustgi

Research output: Contribution to journalArticlepeer-review

146 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)470-483
Number of pages14
JournalCancer Cell
Volume19
Issue number4
DOIs
StatePublished - Apr 12 2011

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cell Biology
  • Cancer Research

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