Obesity, Inflammation, and Tumor Microenvironment in Three-Dimensional Models of Breast Cancer

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Obesity is recognized as a risk factor for breast cancer development and progression. Adipocytes exert their oncogenic effects through complex and interconnected biological mechanisms that encompass metabolic dysfunction, chronic low-grade inflammation, and systemic endocrine alterations. Herein, we reviewed the current evidence explaining how obesity induces a state that reprograms adipose tissue and remodels the breast cancer tumor microenvironment (TME). We first discuss the systemic and local mechanisms linking obesity to inflammation and how these alterations reshape the functional organization of the mammary gland. Then, we discuss how the chronic exposure to tumor-derived signals, together with the altered metabolic state of obese adipose tissue, induces a functional reprogramming of adipocytes, giving rise to so-called cancer-associated adipocytes (CAAs), which actively contribute to tumor progression. Also, the strengths and limitations of biological models to study the crosstalk between adipocytes and tumor cells, including two-dimensional (2D) monolayers and three-dimensional (3D) cell cultures, as well as animal models, are discussed. Special emphasis is placed on 3D co-culture models, which more accurately reproduce spatial organization, direct cell-cell contact, and diffusion dynamics, providing a more physiologically relevant environment for studying how obesity

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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