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Cited by 212Angiogenesis and VEGF in CancerCancer Cells and MetastasisTGF-β signaling in diseases

Tumor microenvironment and angiogenesis

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Nyberg, Pia·2008·Frontiers in Bioscience
DOI 10.2741/3173
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Abstract

The tumor microenvironment is a mixture of extracellular matrix molecules, tumor cells, endothelial cells, fibroblasts and immune cells. Tumor growth and metastasis formation are dependent on the growth of blood vessels into the tumor mass. The tumor microenvironment contributes to this pathological angiogenic process. The extracellular matrix and basement membranes are a source for endogenous angiogenesis inhibitors, such as endostatin. On the other hand, many extracellular matrix molecules can promote angiogenesis by stabilizing blood vessels and sequestering pro-angiogenic growth factors. The majority of stromal cells in carcinomas are fibroblasts. Carcinoma-associated fibroblasts show a distinct phenotype from normal fibroblasts. The mechanisms how the tumor-associated fibroblasts regulate angiogenesis are not fully known, but they are suggested to be an important source for growth factors and cytokines recruiting endothelial cells. The immune cells, particularly macrophages and neutrophils are another source for angiogenesis-regulating chemokines, growth factors and proteases. Taken together, the tumor microenvironment is a complex unorganized tissue of various cell types and extracellular matrix that can regulate the pathological angiogenic switch.

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  • CAFs are key contributors to ECM remodeling, angiogenesis, and metastasis.

    “These CAFs are characterized by the expression of specific markers, such as desmin and fibroblast activation protein, and are now recognized as key contributors to ECM remodeling, angiogenesis, and metastasis [36,37,38,39,40].”

    From Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis (2025) · cites this paper as [39]

    Section 5 says fibroblasts regulate ECM degradation and reports that CAFs enhance tumor angiogenesis. It also describes CAFs in metastatic sites contributing to angiogenesis, but does not establish that CAFs are key contributors to metastasis itself. Page numbers are unavailable in our copy. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • EMT imparts enhanced migratory and invasive capacity, survival advantage under stress, and increased resistance to apoptotic stimuli.

    “This transition imparts enhanced migratory and invasive capacity, survival advantage under stress, and increased resistance to apoptotic stimuli [39,131,132,133].”

    From Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis (2025) · cites this paper as [39]

    Section 6, “Angiogenesis and Metastasis” (page unavailable), describes EMT as a possible mechanism for acquiring an invasive phenotype that can lead to metastasis. It does not attribute survival under stress or resistance to apoptotic stimuli to EMT. Section 3 discusses survival during hypoxia, but links it to p53 status rather than EMT. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Authors
Nyberg, P.
Affiliations
University of Oulu (FI)
Corresponding author
Nyberg, Pia
ORCID
Nyberg, Pia
Venue
Frontiers in Bioscience
Publisher
IMR Press
Published
2008
Volume
Volume
Issue
13
Pages
6537
ISSN
  • 1093-4715 (ISSN-L)
  • 1093-9946
DOI
10.2741/3173
OpenAlex
W1996785840
Cited by
212
References
0
Citations by year
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FWCI
1.29
Type
journal article
Language
en
Open access
Locations
  • Frontiers in bioscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Suomen Kulttuurirahasto
  • Suomen Hammaslääkäriseura Apollonia
  • Oulun Yliopisto
  • National Institutes of Health (DK 55001)
  • National Institute on Alcohol Abuse and Alcoholism (AA53194)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 62987, DK61688, R01DK062987, DK-55001, R01DK061688, R01DK055001)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
  • Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
tumor microenvironment, tumor angiogenesis, extracellular matrix, endostatin, angiogenesis inhibitors, cancer-associated fibroblasts, tumor-associated macrophages, tumor-associated neutrophils, endothelial cells, basement membrane, chemokines, growth factors, proteolytic enzymes, metastasis, angiogenic switch
MeSH terms
Extracellular Matrix, Humans, Neoplasm Metastasis, Neoplasms, Neovascularization, Pathologic, Integrins, Angiogenesis Inhibitors

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