乳腺癌是全球最常见的恶性肿瘤，截至2020年，仍是女性癌症相关死亡的第二大原因。代谢重编程被广泛认为是恶性的标志，因为它重新调整了多个生物过程，包括糖酵解、氧化磷酸化、糖醛酸途径和脂质代谢，这些过程支持了肿瘤细胞的不懈生长需求，并允许癌细胞的远程转移。乳腺癌细胞已有充分的证据证明它们通过突变或失活内在因素，如c-Myc、TP53、缺氧诱导因子和PI3K/AKT/mTOR途径或与周围的肿瘤微环境进行交流，包括缺氧、细胞外酸化和与免疫细胞、癌相关成纤维细胞和脂肪细胞的相互作用，来重编程其代谢。此外，改变的代谢有助于获得或固有治疗耐药性。因此，有必要迫切了解乳腺癌进展的代谢可塑性，以及决定代谢重编程的机制，这解释了对抗标准治疗的耐药性。此审查旨在说明乳腺癌中的代谢变化及其基本机制，以及在乳腺癌治疗中的代谢干预，旨在为开发乳腺癌新的治疗策略提供方案。 ©2023. 作者以Springer Nature Switzerland AG的独家许可。

Breast cancer is the most common malignant tumor globally as of 2020 and remains the second leading cause of cancer-related death among female individuals worldwide. Metabolic reprogramming is well recognized as a hallmark of malignancy owing to the rewiring of multiple biological processes, notably, glycolysis, oxidative phosphorylation, pentose phosphate pathway, as well as lipid metabolism, which support the demands for the relentless growth of tumor cells and allows distant metastasis of cancer cells. Breast cancer cells are well documented to reprogram their metabolism via mutations or inactivation of intrinsic factors such as c-Myc, TP53, hypoxia-inducible factor, and the PI3K/AKT/mTOR pathway or crosstalk with the surrounding tumor microenvironments, including hypoxia, extracellular acidification and interaction with immune cells, cancer-associated fibroblasts, and adipocytes. Furthermore, altered metabolism contributes to acquired or inherent therapeutic resistance. Therefore, there is an urgent need to understand the metabolic plasticity underlying breast cancer progression as well as to dictate metabolic reprogramming that accounts for the resistance to standard of care. This review aims to illustrate the altered metabolism in breast cancer and its underlying mechanisms, as well as metabolic interventions in breast cancer treatment, with the intention to provide strategies for developing novel therapeutic treatments for breast cancer.© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.