This bidirectional interaction ultimately converges into two core oncogenic axes: one is the RBM47-circFNDC3B-IGF2BP1 imbalance axis, which impedes tumor progression through dual inhibition of FNDC3B expression—achieved by reducing linear transcripts via circularization and competing to block mRNA stability; while the other is the ZMIZ1-AS1-PTBP1-ZMIZ1 stabilization axis that enhances transcript stability for homologous genes via lncRNA-RBP complexes and activates downstream signals associated with proliferation and invasion. The gene discussed is ZMIZ1; the disease is neoplasm.