Abstract
Triple-negative breast cancer (TNBC) represents the most aggressive and therapeutically recalcitrant breast cancer subtype, exhibiting dismal clinical outcomes due to its intrinsic heterogeneity and lack of molecularly targeted treatment options. Emerging evidence has established the autophagy-related proteins (ARPs) as key regulators of TNBC pathogenesis, functioning not only as metabolic gatekeepers but also as multifaceted modulators of malignant transformation, disease progression, and therapeutic responsiveness. These proteins exert diverse functions in TNBC through both canonical autophagy-dependent pathways and non-canonical mechanisms. In this review, we critically examine the pleiotropic functions and molecular mechanisms of ARPs in TNBC progression and therapeutic responsiveness, with special emphasis on their context-dependent roles in both fortifying therapeutic resistance and, paradoxically, creating vulnerabilities for therapeutic exploitation.