Genomic amplification of the distal portion of chromosome 3q, which encodes a number of oncogenic proteins, is one of the most frequent chromosomal abnormalities in malignancy. Here we functionally characterise a non-protein product of the 3q region, the long noncoding RNA (lncRNA) PLANE, which is upregulated in 19 of 20 cancer types through copy number gain as well as E2F1-mediated transcriptional activation. Long-read RNA-seq analysis revealed that the major protein coding variant of the nuclear receptor co-repressor 2 (NCOR2) mRNA, NCOR2-202 that is generated through an alternative 5’ splice site within intron 45, was the most highly upregulated transcript caused by PLANE knockdown. Quantitative visualisation of alternative splicing (AS) frequency using integrated genome viewer (IGV) showed that the frequency of the AS event generating NCOR2-202 was increased, whereas the frequency of the AS events giving rise to other NCOR2 mRNA variants were concurrently reduced in cells with PLANE knockdown. PLANE formed an RNA-RNA duplex with the NCOR2 pre-mRNA and bound to heterogeneous ribonucleoprotein M (hnRNPM), thus facilitating the interaction between hnRNPM and the NCOR2 pre-mRNA at intron 45. Instructively, shRNA knockdown of PLANE enhanced the AS event generating NCOR2-202, recapitulating the effect of silencing hnRNPM. Furthermore, the effect of PLANE knockdown on the AS event was abolished by introduction of a shRNA-resistant PLANE mutant but not by introduction of a PLANE mutant with its binding segment to NCOR2 pre-mRNA deleted. On the other hand, hnRNPM-mediated reduction of the AS event generating NCOR2-202 was reversed by PLANE knockdown. Therefore, facilitation of the binding of hnRNPM with the NCOR2 pre-mRNA by PLANE is necessary for hnRNPM-mediated regulation of NCOR2 pre-mRNA AS. Of note, analysing using the modelling alternative junction inclusion quantification (MAJIQ) that detects and quantifies local splicing variations (LSVs) identified additional 55 significant LSVs caused by PLANE knockdown. Nevertheless, the role of PLANE in promoting cancer cell proliferation and tumorigenicity was found to be largely attributable to its modulatory effects on NCOR2 pre-mRNA AS. Collectively, these results uncover a novel lncRNA-mediated mechanism that regulates AS, with practical implications of interference with PLANE as potential treatment approach in the pan-cancer context.