Insulin/IGF Axis in Breast Cancer: Clinical Evidence and Translational Insights.


Journal

Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414

Informations de publication

Date de publication:
19 01 2021
Historique:
received: 29 12 2020
revised: 17 01 2021
accepted: 18 01 2021
entrez: 22 1 2021
pubmed: 23 1 2021
medline: 24 6 2021
Statut: epublish

Résumé

Breast cancer (BC) is the most common neoplasm in women. Many clinical and preclinical studies investigated the possible relationship between host metabolism and BC. Significant differences among BC subtypes have been reported for glucose metabolism. Insulin can promote tumorigenesis through a direct effect on epithelial tissues or indirectly by affecting the levels of other modulators, such as the insulin-like growth factor (IGF) family of receptors, sex hormones, and adipokines. The potential anti-cancer activity of metformin is based on two principal effects: first, its capacity for lowering circulating insulin levels with indirect endocrine effects that may impact on tumor cell proliferation; second, its direct influence on many pro-cancer signaling pathways that are key drivers of BC aggressiveness. In the present review, the interaction between BC, host metabolism, and patients' prognosis has been reviewed across available literature evidence. Obesity, metabolic syndrome, and insulin resistance are all involved in BC growth and could have a relevant impact on prognosis. All these factors act through a pro-inflammatory state, mediated by cytokines originated in fat tissue, and seem to be related to a higher risk of BC development and worse prognosis.

Sections du résumé

BACKGROUND
Breast cancer (BC) is the most common neoplasm in women. Many clinical and preclinical studies investigated the possible relationship between host metabolism and BC. Significant differences among BC subtypes have been reported for glucose metabolism. Insulin can promote tumorigenesis through a direct effect on epithelial tissues or indirectly by affecting the levels of other modulators, such as the insulin-like growth factor (IGF) family of receptors, sex hormones, and adipokines. The potential anti-cancer activity of metformin is based on two principal effects: first, its capacity for lowering circulating insulin levels with indirect endocrine effects that may impact on tumor cell proliferation; second, its direct influence on many pro-cancer signaling pathways that are key drivers of BC aggressiveness.
METHODS
In the present review, the interaction between BC, host metabolism, and patients' prognosis has been reviewed across available literature evidence.
CONCLUSIONS
Obesity, metabolic syndrome, and insulin resistance are all involved in BC growth and could have a relevant impact on prognosis. All these factors act through a pro-inflammatory state, mediated by cytokines originated in fat tissue, and seem to be related to a higher risk of BC development and worse prognosis.

Identifiants

pubmed: 33477996
pii: biom11010125
doi: 10.3390/biom11010125
pmc: PMC7835955
pii:
doi:

Substances chimiques

Insulin 0
Somatomedins 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

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Auteurs

Federica Biello (F)

Department of Translational Medicine, University of Eastern Piedmont, Via Solaroli 17, 28100 Novara, Italy.

Francesca Platini (F)

Division of Oncology, University Hospital "Maggiore della Carità", 28100 Novara, Italy.

Francesca D'Avanzo (F)

Division of Oncology, University Hospital "Maggiore della Carità", 28100 Novara, Italy.

Carlo Cattrini (C)

Division of Oncology, University Hospital "Maggiore della Carità", 28100 Novara, Italy.

Alessia Mennitto (A)

Division of Oncology, University Hospital "Maggiore della Carità", 28100 Novara, Italy.

Silvia Genestroni (S)

Division of Oncology, University Hospital "Maggiore della Carità", 28100 Novara, Italy.

Veronica Martini (V)

Division of Oncology, University Hospital "Maggiore della Carità", 28100 Novara, Italy.
Lab of Immuno-Oncology, CAAD, Center of Autoimmune and Allergic Disease, University of Eastern Piedmont, 28100 Novara, Italy.

Paolo Marzullo (P)

Department of Translational Medicine, University of Eastern Piedmont, Via Solaroli 17, 28100 Novara, Italy.
Division of General Medicine, IRCCS Istituto Auxologico Italiano, Ospedale S. Giuseppe, 28921 Piancavallo-Verbania, Italy.

Gianluca Aimaretti (G)

Department of Translational Medicine, University of Eastern Piedmont, Via Solaroli 17, 28100 Novara, Italy.

Alessandra Gennari (A)

Department of Translational Medicine, University of Eastern Piedmont, Via Solaroli 17, 28100 Novara, Italy.

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