Review reveals how cancer-associated adipocytes fuel progression and drug resistance in solid tumors, highlighting new metabolic targets for precision oncology.
Key Points
Examine how cancer-associated adipocytes undergo metabolic and phenotypic reprogramming to drive tumor progression, metastasis, and therapy resistance across solid malignancies.
Synthesized molecular and cellular evidence on bidirectional crosstalk between cancer-associated adipocytes and tumors within the microenvironment.
Evaluated oncogenic signaling cascades, metabolic rewiring mechanisms, and systemic drivers including obesity and cancer-associated cachexia.
Cancer-associated adipocytes shift toward fibroblast-like phenotypes, depleting lipid stores via lipolysis to fuel tumor fatty acid oxidation and glycolytic remodeling.
Crosstalk through YAP/TAZ, STAT3, and PI3K/AKT pathways promotes extracellular matrix remodeling, angiogenesis, and chemoresistance, notably in triple-negative breast and pancreatic cancers.
Adipocyte-secreted factors including lipocalin-2 accelerate wasting in cachexia, while chronic obesity-induced inflammation exacerbates pro-tumorigenic microenvironments.