Crosstalk and plasticity driving between cancer-associated fibroblasts and tumor microenvironment: significance of breast cancer metastasis

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Abstract

Cancer-associated fibroblasts (CAFs) are the most abundant stromal cell population in breast tumors. A functionally diverse population of CAFs increases the dynamic complexity of the tumor microenvironment (TME). The intertwined network of the TME facilitates the interaction between activated CAFs and breast cancer cells, which can lead to the proliferation and invasion of breast cells. Considering the special transmission function of CAFs, the aim of this review is to summarize and highlight the crosstalk between CAFs and breast cancer cells in the TME as well as the relationship between CAFs and extracellular matrix (ECM), soluble cytokines, and other stromal cells in the metastatic state. The crosstalk between cancer-associated fibroblasts and tumor microenvironment also provides a plastic therapeutic target for breast cancer metastasis. In the course of the study, the inhibitory effects of different natural compounds on targeting CAFs and the advantages of different drug combinations were summarized. CAFs are also widely used in the diagnosis and treatment of breast cancer. The cumulative research on this phenomenon supports the establishment of a targeted immune microenvironment as a possible breakthrough in the prevention of invasive metastasis of breast cancer.

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The Tumor Microenvironment Innately Modulates Cancer Progression

Dominique C. Hinshaw, Lalita A Shevde (2019)

Cancer development and progression occurs in concert with alterations in the surrounding stroma. Cancer cells can functionally sculpt their microenvironment through the secretion of various cytokines, chemokines, and other factors. This results in a reprogramming of the surrounding cells, enabling them to play a determinative role in tumor survival and progression. Immune cells are important constituents of the tumor stroma and critically take part in this process. Growing evidence suggests that the innate immune cells (macrophages, neutrophils, dendritic cells, innate lymphoid cells, myeloid-derived suppressor cells, and NK cells) as well as adaptive immune cells (T cells and B cells) contribute to tumor progression when present in the tumor microenvironment (TME). Crosstalk between cancer cells and the proximal immune cells ultimately results in an environment that fosters tumor growth and metastasis. Understanding the nature of this dialog will allow for improved therapeutics that simultaneously target multiple components of the TME, increasing the likelihood of favorable patient outcomes.

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The biology and function of fibroblasts in cancer.

Raghu Kalluri (2016)

Among all cells, fibroblasts could be considered the cockroaches of the human body. They survive severe stress that is usually lethal to all other cells, and they are the only normal cell type that can be live-cultured from post-mortem and decaying tissue. Their resilient adaptation may reside in their intrinsic survival programmes and cellular plasticity. Cancer is associated with fibroblasts at all stages of disease progression, including metastasis, and they are a considerable component of the general host response to tissue damage caused by cancer cells. Cancer-associated fibroblasts (CAFs) become synthetic machines that produce many different tumour components. CAFs have a role in creating extracellular matrix (ECM) structure and metabolic and immune reprogramming of the tumour microenvironment with an impact on adaptive resistance to chemotherapy. The pleiotropic actions of CAFs on tumour cells are probably reflective of them being a heterogeneous and plastic population with context-dependent influence on cancer.

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Matrix crosslinking forces tumor progression by enhancing integrin signaling.

Kandice R Levental, Hongmei Yu, Laura Kass … (2010)

Tumors are characterized by extracellular matrix (ECM) remodeling and stiffening. The importance of ECM remodeling to cancer is appreciated; the relevance of stiffening is less clear. We found that breast tumorigenesis is accompanied by collagen crosslinking, ECM stiffening, and increased focal adhesions. Induction of collagen crosslinking stiffened the ECM, promoted focal adhesions, enhanced PI3 kinase (PI3K) activity, and induced the invasion of an oncogene-initiated epithelium. Inhibition of integrin signaling repressed the invasion of a premalignant epithelium into a stiffened, crosslinked ECM and forced integrin clustering promoted focal adhesions, enhanced PI3K signaling, and induced the invasion of a premalignant epithelium. Consistently, reduction of lysyl oxidase-mediated collagen crosslinking prevented MMTV-Neu-induced fibrosis, decreased focal adhesions and PI3K activity, impeded malignancy, and lowered tumor incidence. These data show how collagen crosslinking can modulate tissue fibrosis and stiffness to force focal adhesions, growth factor signaling and breast malignancy.

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Author and article information

Contributors

Changgang Sun:

ORCID: http://orcid.org/0000-0003-0778-8788

scgdoctor@126.com

Jibiao Wu: wujibiao1963@163.com

Qibiao Wu: qbwu@must.edu.mo

Journal

Journal ID (nlm-ta): J Transl Med

Journal ID (iso-abbrev): J Transl Med

Title: Journal of Translational Medicine

Publisher: BioMed Central (London )

ISSN (Electronic): 1479-5876

Publication date (Electronic): 17 November 2023

Publication date PMC-release: 17 November 2023

Publication date Collection: 2023

Volume: 21

Electronic Location Identifier: 827

Affiliations

[1 ]State Key Laboratory of Quality Research in Chinese Medicine, and Faculty of Chinese Medicine, Macau University of Science and Technology, ( https://ror.org/03jqs2n27) Avenida Wai Long, Taipa, 999078 Macau China

[2 ]GRID grid.268079.2, ISNI 0000 0004 1790 6079, College of Traditional Chinese Medicine, , Weifang Medical University, ; Weifang, 261000 China

[3 ]GRID grid.464402.0, ISNI 0000 0000 9459 9325, College of Traditional Chinese Medicine, , Shandong University of Traditional Chinese Medicine, ; Jinan, 250355 China

[4 ]GRID grid.461885.6, Department of Oncology, , Weifang Traditional Chinese Hospital, ; Weifang, 261000 China

Author information

Changgang Sun http://orcid.org/0000-0003-0778-8788

Article

Publisher ID: 4714

DOI: 10.1186/s12967-023-04714-2

PMC ID: 10657029

PubMed ID: 37978384

SO-VID: 349b9ee5-4305-4350-9a99-3c4229039b82

License:

Open Access This 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/. The Creative Commons Public Domain Dedication waiver ( http://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.

History

Date received : 18 August 2023

Date accepted : 9 November 2023

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: 8217422

Award ID: 81973677

Award ID: 82305000

Award Recipient : Cun Liu Changgang Sun

Funded by: FundRef http://dx.doi.org/10.13039/501100007129, Natural Science Foundation of Shandong Province;

Award ID: ZR2021LZY015

Award Recipient : Changgang Sun

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ScienceOpen disciplines: Medicine

Keywords: breast cancer,cancer-associated fibroblasts,tumor microenvironment,metastasis

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ScienceOpen disciplines: Medicine

Keywords: breast cancer, cancer-associated fibroblasts, tumor microenvironment, metastasis

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Crosstalk and plasticity driving between cancer-associated fibroblasts and tumor microenvironment: significance of breast cancer metastasis

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Karger: Oncology

Most cited references 152

The Tumor Microenvironment Innately Modulates Cancer Progression

The biology and function of fibroblasts in cancer.

Matrix crosslinking forces tumor progression by enhancing integrin signaling.

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Cited by 13

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