Genetic variants identified through genome-wide association studies (GWAS) are predominantly non-coding, yet, the contribution of non-coding RNAs to the risk of developing complex diseases is not well established. Using targeted RNA sequencing, we annotated long non-coding RNAs (lncRNAs) transcribed from 1.5-Mb intervals surrounding breast cancer (BC) GWAS signals. We showed that BC risk variants are significantly enriched in lncRNA exons, but not their promoters or introns. Eight hundred and forty-four lncRNAs were genetically linked to BC, either by containing a risk-associated variant in their exon, promoter or distal enhancers (identified through capture HiC), suggesting a subset of these may be implicated in BC development. We performed CRISPR-Cas13d-based knockdown screening of the 844 lncRNAs in one normal and two breast cancer cell lines and identified 20 whose knockdown affects breast epithelial cell proliferation (FDR <0.1; five of which were common in more than 2 cell lines). One of the lncRNAs we identified, called KLNC, contains six highly correlated BC risk variants and is an eQTL for the risk alleles in breast tumours (n=700). Consistent with this, we showed that the half-life of KLNC is significantly reduced in the presence of the risk haplotype, revealing a mechanism by which non-coding variants alter lncRNA expression and disease risk. Using antisense oligonucleotides, we confirmed that knockdown of KLNC promotes cell proliferation in ER+ a breast cancer cell-line. Conversely, CRISPRa-based overexpression of KLNC halted cell proliferation by inducing a G2/M phase cell cycle arrest in cancer cell lines but not normal cell lines. KLNC pull-down identified multiple proteins that bind the lncRNA, including several involved in RNA processing and DNA replication. Experiments are now being conducted to explore the mechanism further and establish the role of KLNC in DNA replication, thus explaining its effect on cell proliferation.