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Autophagy plays paradoxical roles in breast cancer, functioning as both a stress-adaptive survival mechanism and a tumor-suppressive process depending on cellular and microenvironmental context. However, the molecular logic governing this functional duality has remained incompletely understood. Emerging evidence identifies the Wnt/β-catenin-mTOR axis as a central signaling hub that integrates proliferative, metabolic, and developmental cues to determine the directionality and functional outcome of autophagy. Aberrant activation of Wnt/β-catenin signaling reinforces mTOR activity, suppresses autophagic flux, and promotes stemness, epithelial-mesenchymal transition, therapeutic resistance, and immune evasion. Conversely, inhibition of Wnt signaling can relieve mTOR-mediated autophagy repression, leading to context-dependent induction of cytotoxic or cytostatic autophagy. Beyond tumor cell-intrinsic effects, Wnt-mTOR-autophagy crosstalk critically shapes the tumor immune microenvironment. In particular, SOCS3 deficiency-driven activation of Wnt/mTOR signaling represses autophagy in early-stage myeloid-derived suppressor cells, thereby sustaining their survival and immunosuppressive function. This mechanism highlights autophagy as an immunometabolic fate switch that governs myeloid cell persistence and antitumor immune suppression. Importantly, autophagy also feeds back to restrain Wnt signaling through selective degradation of pathway components, establishing dynamic regulatory loops that fine-tune oncogenic signaling output. In this review, we synthesize current evidence to delineate the bidirectional crosstalk between Wnt/β-catenin signaling, mTOR activity, and autophagy in breast cancer. We discuss how this integrated network governs tumor cell states, immune suppression, and therapeutic responsiveness, and propose a biomarker-driven, context-specific framework for autophagy modulation. By integrating signaling, autophagy flux, and myeloid immune status, precision targeting of the Wnt-mTOR-autophagy axis may offer new opportunities to overcome therapeutic resistance and improve clinical outcomes in breast cancer.