Adipocytes are the main stromal cells in the tumor microenvironment. In addition to serving as energy stores for triglycerides, adipocytes may function as an active endocrine organ. The crosstalk between adipocytes and cancer cells was shown to promote the migration, invasion and proliferation of cancer cells and to cause phenotypic and functional changes in adipocytes. Tumor‑derived soluble factors, such as TNF‑α, plasminogen activator inhibitor 1, Wnt3a, IL‑6, and exosomal microRNAs (miRNA/miRs), including miR‑144, miR‑126, miR‑155, as well as other miRNAs, have been shown to act on adipocytes at the tumor invasion front, resulting in the formation of cancer‑associated adipocytes (CAAs) with diminished reduced terminal differentiation markers and a dedifferentiated phenotype. In addition, the number and size of CAA lipid droplets have been found to be significantly reduced compared with those of mature adipocytes, whereas inflammatory cytokines and proteases are overexpressed. The aim of the present review was to summarize the latest findings on the biological changes of CAAs and the potential role of tumor‑adipocyte crosstalk in the formation of CAAs, in the hope of providing novel perspectives for breast cancer treatment.

中文翻译：

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癌症相关脂肪细胞形成的分子机制概述（综述）。

脂肪细胞是肿瘤微环境中的主要基质细胞。除了作为甘油三酯的能量储存器外，脂肪细胞还可以作为一个活跃的内分泌器官。脂肪细胞和癌细胞之间的串扰被证明可以促进癌细胞的迁移、侵袭和增殖，并引起脂肪细胞的表型和功能变化。肿瘤衍生的可溶性因子，例如 TNF-α、纤溶酶原激活物抑制剂 1、Wnt3a、IL-6 和外泌体 microRNA (miRNA/miR)，包括 miR-144、miR-126、miR-155 以及其他 miRNA ，已被证明作用于肿瘤侵袭前沿的脂肪细胞，导致癌症相关脂肪细胞 (CAA) 的形成，其终末分化标志物减少和去分化表型减少。此外，与成熟脂肪细胞相比，CAA 脂滴的数量和大小显着减少，而炎性细胞因子和蛋白酶过表达。本综述旨在总结CAA生物学变化的最新发现以及肿瘤-脂肪细胞串扰在CAA形成中的潜在作用，以期为乳腺癌治疗提供新的视角。