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c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment
The MYC oncogenic family is dysregulated in diverse tumors which is generally linked to the poor prognosis of tumors. The members in MYC family are transcription factors which are responsible for the regulation of various genes expression. Among them, c-MYC is closely related to the progression of t...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9887805/ https://www.ncbi.nlm.nih.gov/pubmed/36721232 http://dx.doi.org/10.1186/s12964-023-01043-1 |
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author | Gao, Fang-yan Li, Xin-tong Xu, Kun Wang, Run-tian Guan, Xiao-xiang |
author_facet | Gao, Fang-yan Li, Xin-tong Xu, Kun Wang, Run-tian Guan, Xiao-xiang |
author_sort | Gao, Fang-yan |
collection | PubMed |
description | The MYC oncogenic family is dysregulated in diverse tumors which is generally linked to the poor prognosis of tumors. The members in MYC family are transcription factors which are responsible for the regulation of various genes expression. Among them, c-MYC is closely related to the progression of tumors. Furthermore, c-MYC aberrations is tightly associated with the prevalence of breast cancer. Tumor microenvironment (TME) is composed of many different types of cellular and non-cellular factors, mainly including cancer-associated fibroblasts, tumor-associated macrophages, vascular endothelial cells, myeloid-derived suppressor cells and immune cells, all of which can affect the diagnosis, prognosis, and therapeutic efficacy of breast cancer. Importantly, the biological processes occurred in TME, such as angiogenesis, immune evasion, invasion, migration, and the recruition of stromal and tumor-infiltrating cells are under the modulation of c-MYC. These findings indicated that c-MYC serves as a critical regulator of TME. Here, we aimed to summarize and review the relevant research, thus to clarify c-MYC is a key mediator between breast cancer cells and TME. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01043-1. |
format | Online Article Text |
id | pubmed-9887805 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-98878052023-02-01 c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment Gao, Fang-yan Li, Xin-tong Xu, Kun Wang, Run-tian Guan, Xiao-xiang Cell Commun Signal Review The MYC oncogenic family is dysregulated in diverse tumors which is generally linked to the poor prognosis of tumors. The members in MYC family are transcription factors which are responsible for the regulation of various genes expression. Among them, c-MYC is closely related to the progression of tumors. Furthermore, c-MYC aberrations is tightly associated with the prevalence of breast cancer. Tumor microenvironment (TME) is composed of many different types of cellular and non-cellular factors, mainly including cancer-associated fibroblasts, tumor-associated macrophages, vascular endothelial cells, myeloid-derived suppressor cells and immune cells, all of which can affect the diagnosis, prognosis, and therapeutic efficacy of breast cancer. Importantly, the biological processes occurred in TME, such as angiogenesis, immune evasion, invasion, migration, and the recruition of stromal and tumor-infiltrating cells are under the modulation of c-MYC. These findings indicated that c-MYC serves as a critical regulator of TME. Here, we aimed to summarize and review the relevant research, thus to clarify c-MYC is a key mediator between breast cancer cells and TME. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01043-1. BioMed Central 2023-01-31 /pmc/articles/PMC9887805/ /pubmed/36721232 http://dx.doi.org/10.1186/s12964-023-01043-1 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Review Gao, Fang-yan Li, Xin-tong Xu, Kun Wang, Run-tian Guan, Xiao-xiang c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment |
title | c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment |
title_full | c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment |
title_fullStr | c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment |
title_full_unstemmed | c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment |
title_short | c-MYC mediates the crosstalk between breast cancer cells and tumor microenvironment |
title_sort | c-myc mediates the crosstalk between breast cancer cells and tumor microenvironment |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9887805/ https://www.ncbi.nlm.nih.gov/pubmed/36721232 http://dx.doi.org/10.1186/s12964-023-01043-1 |
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