胰腺癌（PC）是全球最致命的恶性肿瘤之一，其原因是诊断延迟和对当前治疗的耐药性。胰腺肿瘤细胞与其肿瘤微环境（TME）之间的相互作用使癌细胞能够逃脱抗癌治疗，导致PC难以治疗。脂肪组织具有内分泌功能和脂质储存能力，能够维持能量平衡。脂肪细胞和PC细胞之间的直接或间接相互作用导致脂肪细胞功能障碍，表现为形态改变、脂肪丢失、异常脂因子分泌和成纤维细胞样转化。从功能失调的脂肪细胞释放的各种脂因子已被报道能够通过不同机制促进PC细胞的增殖、侵袭、转移、干细胞特性和化疗耐药性。脂肪细胞释放的额外脂质可以进入TME，从而改变PC细胞和周围基质细胞的代谢。此外，转分化潜能使脂肪细胞转化为各种细胞类型，可能引起炎症反应和细胞外基质重组，以调节肿瘤负担。了解脂肪细胞在PC中促肿瘤功能的分子基础可能提供新的治疗靶点。

Pancreatic cancer (PC) remains one of the most lethal malignancies across the world, which is due to delayed diagnosis and resistance to current therapies. The interactions between pancreatic tumor cells and their tumor microenvironment (TME) allow cancer cells to escape from anti-cancer therapies, leading to difficulties in treating PC. With endocrine function and lipid storage capacity, adipose tissue can maintain energy homeostasis. Direct or indirect interaction between adipocytes and PC cells leads to adipocyte dysfunction characterized by morphological change, fat loss, abnormal adipokine secretion, and fibroblast-like transformation. Various adipokines released from dysfunctional adipocytes have been reported to promote proliferation, invasion, metastasis, stemness, and chemoresistance of PC cells via different mechanisms. Additional lipid outflow from adipocytes can be taken into the TME and thus alter the metabolism in PC cells and surrounding stromal cells. Besides, the trans-differentiation potential enables adipocytes to turn into various cell types, which may give rise to an inflammatory response as well as extracellular matrix reorganization to modulate tumor burden. Understanding the molecular basis behind the protumor functions of adipocytes in PC may offer new therapeutic targets.© The author(s).