Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University, Nanchang 330006, China.
Department of Breast Surgery, Jiangxi Cancer Hospital, Nanchang 330029, China.
J Mol Cell Biol. 2023 Aug 3;15(4). doi: 10.1093/jmcb/mjad025.
Recent studies have demonstrated that cancer-associated adipocytes (CAAs) in the tumor microenvironment are involved in the malignant progression of breast cancer. However, the underlying mechanism of CAA formation and its effects on the development of breast cancer are still unknown. Here, we show that CSF2 is highly expressed in both CAAs and breast cancer cells. CSF2 promotes inflammatory phenotypic changes of adipocytes through the Stat3 signaling pathway, leading to the secretion of multiple cytokines and proteases, particularly C-X-C motif chemokine ligand 3 (CXCL3). Adipocyte-derived CXCL3 binds to its specific receptor CXCR2 on breast cancer cells and activates the FAK pathway, enhancing the mesenchymal phenotype, migration, and invasion of breast cancer cells. In addition, a combination treatment targeting CSF2 and CXCR2 shows a synergistic inhibitory effect on adipocyte-induced lung metastasis of mouse 4T1 cells in vivo. These findings elucidate a novel mechanism of breast cancer metastasis and provide a potential therapeutic strategy for breast cancer metastasis.
最近的研究表明,肿瘤微环境中的癌症相关脂肪细胞(CAAs)参与了乳腺癌的恶性进展。然而,CAA 形成的潜在机制及其对乳腺癌发展的影响仍不清楚。在这里,我们表明 CSF2 在 CAA 和乳腺癌细胞中均高度表达。CSF2 通过 Stat3 信号通路促进脂肪细胞的炎症表型改变,导致多种细胞因子和蛋白酶的分泌,特别是 C-X-C 基序趋化因子配体 3(CXCL3)。脂肪细胞衍生的 CXCL3 与乳腺癌细胞上其特异性受体 CXCR2 结合并激活 FAK 途径,增强乳腺癌细胞的间充质表型、迁移和侵袭。此外,针对 CSF2 和 CXCR2 的联合治疗对体内小鼠 4T1 细胞脂肪细胞诱导的肺转移具有协同抑制作用。这些发现阐明了乳腺癌转移的新机制,并为乳腺癌转移提供了一种潜在的治疗策略。