ArticleCell death & disease2026
CRMP2 inhibits metastasis formation by impairing ILF3-dependent stabilization of CXCL10 mRNA in breast cancer.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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. Mechanistically, CRMP2 overexpression leads to downregulation of CXCL10. We also found that the correlation between CRMP2 and CXCL10 is mediated by interleukin enhancer-binding factor 3 (ILF3). The D-hydantoinases (D-HYD) fragment of CRMP2 specifically interacts with the second double-stranded RNA binding motif (dsRBM2) of ILF3. Overexpressed CRMP2 reduces the expression of ILF3 in proteasome-dependent degradation via Lys 48-linked polyubiquitination at Lys
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