Division of Gastroenterology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Cancer Cell. 2011 Apr 12;19(4):470-83. 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.
p120-catenin（p120ctn）与 E-cadherin 相互作用，但据我们所知，目前还没有正式的证据表明 p120ctn 是一种真正的肿瘤抑制基因。我们在此报告，p120ctn 的缺失会导致小鼠发生肿瘤。我们已经构建了 p120ctn 的条件性敲除模型，该模型的小鼠在口腔、食管和鳞状前胃中会发展出前瘤和肿瘤病变。肿瘤衍生的细胞分泌粒细胞巨噬细胞集落刺激因子（GM-CSF）、巨噬细胞集落刺激因子（M-CSF）、单核细胞趋化蛋白-1（MCP-1）和肿瘤坏死因子-α（TNFα）。肿瘤含有显著的纤维组织增生和免疫细胞浸润。未成熟的髓样细胞构成了存在的免疫细胞的很大一部分，可能参与了促进有利的肿瘤微环境，包括成纤维细胞的激活。
