Breast cancer GWAS have identified three independent signals at 18q11 associated with risk. Most post-GWAS functional studies assess the impact of genetic variants on enhancers and nearby protein-coding genes. We recently discovered that another mechanism by which variants modify risk is through altered expression or function of long noncoding RNAs (lncRNAs). Using RNA Captureseq and eQTL analyses, we identified a novel lncRNA (called K-LNC) at 18q11 that is an eQTL overlapping the signal 3 risk variants. K-LNC is a 6.7kb, single exon, nuclear-restricted lncRNA derived from the intron of KCTD1-T5, an uncharacterised isoform of the transcriptional repressor, KCTD1. Variant capture-HiC showed that signals 1 and 2 overlapped putative enhancers that looped to the KCTD1-5 promoter, providing further support that K-LNC/KCTD1-T5 are the target genes at 18q11. Consistent with the eQTL results, mRNA stability assays in heterozygous breast cell lines showed that K-LNC has a significantly shorter half-life in the presence of the risk haplotype. CRISPR-activation of the KCTD1-T5/K-LNC promoter induced apoptosis in cancer cell lines. In Hs578T cancer cells, K-LNC but not KCTD1-T5 overexpression induced rapid cell death via apoptosis, suggesting that K-LNC has an independent function to KCTD1-T5. In MCF7 and MDAMB231 cancer cells, overexpression of K-LNC or KCTD1-T5 strongly inhibited cell proliferation and colony formation via apoptosis. Importantly, K-LNC/KCTD1-T5-induced apoptosis was not observed in three normal breast cell lines, suggesting that ectopic K-LNC expression could be exploited for breast cancer treatment. Transcriptomic analyses based on RNAseq in MCF7 cells overexpressing K-LNC identified splicing, response to hormone and ubiquitin-like (Ubl) conjugation as enriched functional categories. Consistent with this, RNA pulldown of K-LNC followed by mass spectrometry identified an enrichment in proteins associated with splicing, Ubl conjugation and DNA damage response. In summary, our results emphasize that modulation of lncRNA expression or function may be prominent mechanisms underlying complex traits.