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Preclinical studies demonstrate CCL5's role in breast cancer progression, indicating potential therapeutic targets.
CCL5, abbreviated from C–C motif chemokine ligand 5, exerts diverse regulatory effects on both the initiation and progression of breast cancer (BC), making it a focal point of extensive research within the field. By enhancing the growth, invasive ability, and metastatic potential of BC cells, simultaneously recruiting and polarizing immunosuppressive cell populations, CCL5 actively reshapes the tumor immune microenvironment. Furthermore, elevated CCL5 levels are strongly linked to particular clinicopathological parameters, worse clinical outcomes, and a higher likelihood of recurrence in BC, suggesting its value in early diagnosis and prognosis. Current preclinical studies targeting the CCL5/CCR5 axis have demonstrated notable efficacy in inhibiting the progression of BC. This article explores how CCL5 contributes to BC progression and elucidates its regulatory mechanisms, providing theoretical support and potential targets for innovative therapeutic approaches.
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Mu et al. (2026) studied this question.
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