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Abstract Tumor-derived elements contribute to the formation of the pre-metastatic niche (PMN) and facilitate cancer metastasis, but much less is known about the key molecular mechanisms. Here, we demonstrate that collapsin response mediator protein 2 (CRMP2), a critical regulator of the cytoskeleton, is associated with metastasis in breast cancer. CRMP2 overexpression inhibits both lung metastasis and PMN formation in breast cancer.
1 Introduction In the context of T regulatory lymphocytes, innate Treg (nTreg, or natural Treg, which leaves the thymus in the form of mature cells) and acquired Treg (iTreg, induced Treg, generated by naive CD4+ T response to antigenic stimulation) have been characterized (1). These cell types may exert their immunoregulatory activity directly by cell-to-cell contact, releasing immunosuppressive cytokines, or induction of apoptosis (1).
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