ArticleCancer cell2011
Deletion of p120-catenin results in a tumor microenvironment with inflammation and cancer that establishes it as a tumor suppressor gene.
Article in Cancer cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.
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Who cites it
133 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
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- Cellular Origins and Lineage Plasticity in Cancer.Cold Spring Harbor perspectives in medicine · 2024Review
- Expression of p120 - catenin in oral squamous cell carcinoma and apparently normal mucosa adjacent to oral squamous cell carcinoma.Journal of clinical and experimental dentistry · 2024Article
- Functions of p120-catenin in physiology and diseases.Frontiers in molecular biosciences · 2024Review
- Key Genetic Determinants Driving Esophageal Squamous Cell Carcinoma Initiation and Immune Evasion.Gastroenterology · 2023Article
- IL-1β transgenic mouse model of inflammation driven esophageal and oral squamous cell carcinoma.Scientific reports · 2023Article
- Esophageal organoids: applications and future prospects.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Preoperative systemic immune-inflammation index for predicting the prognosis of thymoma with radical resection.Thoracic cancer · 2023Article
- Construction and Quantitative Evaluation of a Tissue-Specific Sleeping Beauty by EDL2-Specific Transposase Expression in Esophageal Squamous Carcinoma Cell Line KYSE-30.Molecular biotechnology · 2023Article
73 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 7 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.