Adipokines as endocrine, paracrine, and autocrine factors in breast cancer risk and progression
Open accessAbstract
Adipokines (leptin, adiponectin, and hepatocyte growth factor (HGF)) secreted from adipose tissue have come to be recognized for their contribution to the mechanisms by which obesity and related metabolic disorders influence breast cancer risk. In this review, we discuss the direct and indirect effects of these protein factors on the biological and clinical aspects of breast cancer biology, and emphasize their distinctive modes of action through endocrine-, paracrine-, and autocrine-mediated pathways. The stimulatory effects of leptin on breast cancer growth were considered to occur primarily via activation of the estrogen receptor; however, new evidence suggests that leptin may be acting on downstream cell signaling pathways in both estrogen-dependent and -independent cell types. Another secretory adipokine, HGF, may act largely not only to promote tumor cell invasion, but also to enhance tumor growth indirectly by stimulating angiogenesis. In contrast, adiponectin, an endogenous insulin sensitizer, exerts a direct growth-inhibitory effect on tumor cells by downregulating cell proliferation and upregulating apoptosis, and also inhibits tumor-related angiogenesis.
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Some studies have suggested anti-angiogenic properties for adiponectin, but these studies rely on recombinant preparations of the protein, and the quality of these preparations varies widely.
“Some studies have suggested anti-angiogenic properties for adiponectin (72), but these studies rely on recombinant preparations of the protein, and the quality of these preparations varies widely.”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [72]
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Flagged first, then by citations
Research works printed but not linked: 3
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- Authors
- Vona-Davis, L., & Rose, D. P.
- Affiliations
- West Virginia University (US)
- ORCID
- Vona-Davis, Linda
- Venue
- Endocrine-Related Cancer
- Publisher
- Bioscientifica
- Published
- 2007-06-01
- Volume
- 14
- Issue
- 2
- Pages
- 189-206
- ISSN
- 1351-0088 (ISSN-L)
- 1479-6821
- OpenAlex
- W2129731670
- Cited by
- 496
- References
- 145
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 8 · 2023: 9 · 2022: 10 · 2021: 14 · 2020: 22 · 2019: 22 · 2018: 27 · 2017: 54 · 2016: 29 · 2015: 42 · 2014: 28 · 2013: 53 · 2012: 36
- FWCI
- 3.76
- Type
- journal article
- Language
- en
- Update notices
- correction (2011-10-01)
- Open access
- bronze
- doi.org
- Locations
- Endocrine Related Cancer (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Oncology › Cancer Risks and Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- adipokines, breast cancer, leptin, adiponectin, hepatocyte growth factor, obesity, hormone signaling, paracrine signaling, autocrine signaling, estrogen receptor, tumor angiogenesis, tumor invasion, apoptosis, cell proliferation, insulin sensitivity
- MeSH terms
- Breast Neoplasms, Female, Humans, Risk, Hepatocyte Growth Factor, Disease Progression, Autocrine Communication, Paracrine Communication, Leptin, Adiponectin
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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