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Abstract

AMD3100 (Plerixafor), a specific antagonist of CXCR4, is the most potent small molecule non-peptide inhibitor to CXCR4/CXCL12 axis. The chemokine receptor CXCR4 and its ligand CXCL12 (SDF-1) expressed in a variety of tumor cells play an important role in regulating tumor biological behavior. The tumor microenvironment (TME) is the environment around a tumor, comprising blood vessels, immune cells, fibroblasts, signaling molecules and the extracellular matrix which are involved in tumor growth, invasion, metastasis, immune escape and tumor eradication. Although AMD3100 has been intensively investigated in tumor biology, it remains unclear how this treatment regimen modulates immune cells in the TME, which in turn affects the antitumor efficacy of other therapies. In this review, we specifically revisit the evidence from our and others' studies that AMD3100 acts as an immunomodulator to regulate immune responses in the TME and provide the perspective of synergy of AMD3100 with other therapeutics to prevent tumor development, progression, and metastasis.