Adipocytes as Orchestrators of Multimodal Cancer Therapy Resistance

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)

The emergence of therapy resistance remains a formidable barrier to successful clinical outcomes in oncology, necessitating a deeper understanding of the tumor microenvironment (TME) as a dynamic ecosystem. Adipocytes, once viewed as passive energy reservoirs, are now recognized as active orchestrators of tumor progression and multimodal therapy resistance, particularly in adipose-rich malignancies. This review comprehensively delineates the multifaceted mechanisms through which adipocytes shield cancer cells from therapeutic insults, including chemotherapy, targeted agents, and immunotherapies. We analyze the clinical evidence positioning visceral adiposity as a critical determinant of treatment failure and explore the complex molecular interplay driven by the adipocyte-derived secretome, lipid metabolite-mediated metabolic rewiring, and the horizontal transfer of bioactive cargo via adipocyte-derived extracellular vesicles, and adipocyte-mediated remodeling of the TME. Furthermore, we highlight noncanonical roles such as direct organelle donation, lipid-mediated drug sequestration, the enhancement of DNA repair pathways, and the activation of cell adhesion-dependent survival signaling. We also synthesize recent technological advancements employed to interrogate the intricate adipocyte-cancer interaction. Finally, we discuss emerging therapeutic strategies aimed at disrupting

Evidence level

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

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