乳腺癌是一种异质性疾病，其肿瘤细胞亚群被称为乳腺癌干细胞 (BCSC)，具有自我更新和分化能力，在肿瘤的发生、进展和治疗抵抗中发挥着关键作用。肿瘤微环境（TME）是一个复杂的区域，其中存在多种癌细胞，与分泌因子和细胞外基质形成高度相互作用的环境。自噬是一种细胞自我消化过程，影响肿瘤 TME 中的动态细胞过程，整合调节肿瘤发展和异质性的多种信号。自噬在乳腺 TME 中是一把双刃剑，具有促肿瘤和抑制肿瘤的作用。自噬通过调节肿瘤细胞存活、迁移和侵袭、代谢重编程和上皮间质转化（EMT）来促进乳腺肿瘤发生。 BCSC 利用自噬来维持干性特性、逃避免疫监视并抵抗治疗干预。相反，过度或失调的自噬可能导致 BCSC 分化或细胞死亡，这为治疗探索提供了潜在的途径。 BCSCs 中调节自噬的分子机制，包括哺乳动物雷帕霉素靶蛋白 (mTOR)、AMPK 和 Beclin-1 信号通路，可能是乳腺癌药物干预的潜在靶点。这篇综述全面概述了自噬和 BCSC 之间的关系，强调了我们对它们相互作用的理解的最新进展。我们还讨论了自噬靶向药物的现状及其在 BCSC 中的临床前和临床开发。

Breast cancer is a heterogeneous disease, with a subpopulation of tumor cells known as breast cancer stem cells (BCSCs) with self-renewal and differentiation abilities that play a critical role in tumor initiation, progression, and therapy resistance. The tumor microenvironment (TME) is a complex area where diverse cancer cells reside creating a highly interactive environment with secreted factors, and the extracellular matrix. Autophagy, a cellular self-digestion process, influences dynamic cellular processes in the tumor TME integrating diverse signals that regulate tumor development and heterogeneity. Autophagy acts as a double-edged sword in the breast TME, with both tumor-promoting and tumor-suppressing roles. Autophagy promotes breast tumorigenesis by regulating tumor cell survival, migration and invasion, metabolic reprogramming, and epithelial-mesenchymal transition (EMT). BCSCs harness autophagy to maintain stemness properties, evade immune surveillance, and resist therapeutic interventions. Conversely, excessive, or dysregulated autophagy may lead to BCSC differentiation or cell death, offering a potential avenue for therapeutic exploration. The molecular mechanisms that regulate autophagy in BCSCs including the mammalian target of rapamycin (mTOR), AMPK, and Beclin-1 signaling pathways may be potential targets for pharmacological intervention in breast cancer. This review provides a comprehensive overview of the relationship between autophagy and BCSCs, highlighting recent advancements in our understanding of their interplay. We also discuss the current state of autophagy-targeting agents and their preclinical and clinical development in BCSCs.