Obesity has been linked to the increased risk and aggressiveness of many types of carcinoma. A state of chronic inflammation in adipose tissue (AT), resulting in genotoxic stress, may contribute to carcinogenesis and cancer initiation. Evidence that AT plays a role in cancer aggressiveness is solid and mounting. During cancer progression, tumor cells engage in a metabolic symbiosis with adjacent AT. Mature adipocytes provide adipokines and lipids to cancer cells, while stromal and immune cells from AT infiltrate carcinomas and locally secrete paracrine factors within the tumor microenvironment. This review focuses on the crosstalk between AT and tumor cells that promotes tumor growth and increases cellular lipid metabolism, metastasis, and chemoresistance.

肥胖与多种癌症的风险和侵袭性增加有关。脂肪组织（AT）的慢性炎症状态会导致基因毒性应激，可能会导致癌变和癌症发生。越来越多的证据表明 AT 在癌症侵袭性中发挥作用。在癌症进展过程中，肿瘤细胞与邻近的 AT 发生代谢共生。成熟的脂肪细胞为癌细胞提供脂肪因子和脂质，而来自 AT 的基质细胞和免疫细胞则浸润癌并在肿瘤微环境中局部分泌旁分泌因子。本综述重点关注 AT 和肿瘤细胞之间的串扰，这种串扰促进肿瘤生长并增加细胞脂质代谢、转移和化疗耐药性。