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Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers
PURPOSE: In the course of tumor progression, cancer clones interact with host normal cells, and these interactions make them under selection pressure all the time. Cell competition, which can eliminate suboptimal cells and optimize organ development via comparison of cell fitness information, is fou...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9261164/ https://www.ncbi.nlm.nih.gov/pubmed/35796779 http://dx.doi.org/10.1007/s00432-022-04143-6 |
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author | Yu, Jing Zhang, Yamin Zhu, Huiyong |
author_facet | Yu, Jing Zhang, Yamin Zhu, Huiyong |
author_sort | Yu, Jing |
collection | PubMed |
description | PURPOSE: In the course of tumor progression, cancer clones interact with host normal cells, and these interactions make them under selection pressure all the time. Cell competition, which can eliminate suboptimal cells and optimize organ development via comparison of cell fitness information, is found to take place between host cells and transformed cells in mammals and play important roles in different phases of tumor progression. The aim of this study is to summarize the current knowledge about the roles and corresponding mechanisms of different cell competition interactions between host normal cells and transformed cells involved in mammalian tumor development. METHODS: We reviewed the published relevant articles in the Pubmed. RESULTS: So far, the role of several cell competition interactions have been well described in the different phases of mammalian tumor genesis and development. While cell competitions for trophic factors and epithelial defense against cancer (EDAC) prevent the emergence of transformed cells and suppress carcinogenesis, fitness-fingerprints-comparison system and Myc supercompetitors promote the local expansion of transformed cells after the early tumor lesion is formatted. In addition, various preclinical tumor-suppression models which based on the molecular mechanisms of these competition interactions show potential clinical value of boosting the fitness of host normal cells. CONCLUSION: Cell competition between host and transformed cells has pleiotropic effects in mammalian tumor genesis and development. The clarification of specific molecular mechanisms shed light on novel ideas for the prevention and treatment of cancer. |
format | Online Article Text |
id | pubmed-9261164 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-92611642022-07-07 Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers Yu, Jing Zhang, Yamin Zhu, Huiyong J Cancer Res Clin Oncol Review PURPOSE: In the course of tumor progression, cancer clones interact with host normal cells, and these interactions make them under selection pressure all the time. Cell competition, which can eliminate suboptimal cells and optimize organ development via comparison of cell fitness information, is found to take place between host cells and transformed cells in mammals and play important roles in different phases of tumor progression. The aim of this study is to summarize the current knowledge about the roles and corresponding mechanisms of different cell competition interactions between host normal cells and transformed cells involved in mammalian tumor development. METHODS: We reviewed the published relevant articles in the Pubmed. RESULTS: So far, the role of several cell competition interactions have been well described in the different phases of mammalian tumor genesis and development. While cell competitions for trophic factors and epithelial defense against cancer (EDAC) prevent the emergence of transformed cells and suppress carcinogenesis, fitness-fingerprints-comparison system and Myc supercompetitors promote the local expansion of transformed cells after the early tumor lesion is formatted. In addition, various preclinical tumor-suppression models which based on the molecular mechanisms of these competition interactions show potential clinical value of boosting the fitness of host normal cells. CONCLUSION: Cell competition between host and transformed cells has pleiotropic effects in mammalian tumor genesis and development. The clarification of specific molecular mechanisms shed light on novel ideas for the prevention and treatment of cancer. Springer Berlin Heidelberg 2022-07-07 2023 /pmc/articles/PMC9261164/ /pubmed/35796779 http://dx.doi.org/10.1007/s00432-022-04143-6 Text en © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Review Yu, Jing Zhang, Yamin Zhu, Huiyong Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers |
title | Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers |
title_full | Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers |
title_fullStr | Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers |
title_full_unstemmed | Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers |
title_short | Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers |
title_sort | pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9261164/ https://www.ncbi.nlm.nih.gov/pubmed/35796779 http://dx.doi.org/10.1007/s00432-022-04143-6 |
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