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

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

来源：Cancer Cell, 2011, 19(4): 470-483.

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-alpha (TNF alpha). 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.

• 出版日期2011-4-12