IGF2BP3 and neoplasm: Similar phenomena were also observed in the mouse in-vein metastasis model where wild-type circITGB6, rather than the IGF2BP3 interaction-deficient circITGB6 mutant, promoted tumor metastasis (Supplementary Fig. 6d), increased metastatic nodules in the lungs (Supplementary Fig. 6e) and facilitated EMT process in metastatic nodules (Supplementary Fig. 6f), further supporting the contribution of the interaction between circITGB6 and IGF2BP3 on tumor metastasis.