Gene gating is a post-transcriptional gene regulation process whereby transcriptionally active genes tether to the nuclear pore complex for rapid mRNAs export into the cytoplasm. Our study first demonstrated this process in mammalian cells, showing that a colorectal oncogenic super-enhancer (OSE) increases MYC expression post-transcriptionally, via a stepwise repositioning of the MYC gene towards the nuclear pores1,2. The enhanced proximity of MYC gene to the nuclear pores enabled faster MYC mRNA export to the cytoplasm, to escape degradation in the nucleus. This gene gating mechanism is modulated by WNT signaling, which promotes the recruitment of the pore-associated factors AHCTF1 and NUP133 to a CTCF binding site (CTCFBS) within the OSE. Mutation of this CTCFBS within the OSE reduces the expression of the CCAT1 eRNA previously shown to regulate MYC, disrupts the recruitment of OSE and MYC to the nuclear pores, and subsequently decreases both MYC transcripts export and cell proliferation. To access whether the gating process also occurs in intact tumor tissues, we employed the Chromatin in situ proximity (ChrISP) assay to detect the proximity between the breast cancer-specific OSE regulating MYC and the NUP133 epitopes in luminal A breast tumor sections. Interestingly, we observed prominent ChrISP signals in tumor cells with high levels of NUP133 staining, suggesting that gene gating operates within the tissue microenvironment of breast tumors. Moreover, endothelial cells also displayed a prominent OSE-NUP133 signal, implicating gene-gating in neo-angiogenesis. In summary, we have uncovered a novel WNT/ß-catenin-AHCTF1-CTCF-eRNA cascade that promotes tumour cell growth via facilitated MYC mRNA export within the 3D nuclear architecture. Our findings highlight the potential of gene gating process as a novel biomarker of tumors and target for therapeutic intervention.