High-grade serous ovarian cancer (HGSOC) is the most common and aggressive form of ovarian cancer. PARP inhibitors (PARPis) have transformed the treatment of homologous recombination (HR)-deficient tumours, particularly those with BRCA1/2 mutations, but many patients exhibit limited responses. Understanding the mechanisms that regulate PARPi response is therefore critical for improving patient outcomes. Our lab has recently identified over 1,000 long noncoding RNAs (lncRNAs) from HGSOC tumours. CRISPR-Cas13d screens in HGSOC cell lines identified one lncRNA, LNC2, that enhances sensitivity to the PARPi, olaparib. LNC2 is a 3,926 bp, 2-exon lncRNA located in an intergenic region on the chr 8. Analysis of >7,000 RNA-seq samples showed that LNC2 is selectively expressed in ovary, cervix and fallopian tube tissues and a subset of ovarian cancers. Antisense oligonucleotide (ASO)-mediated depletion of LNC2 sensitised multiple HGSOC cell lines to olaparib, reducing IC50 values by 2~3-fold, while having minimal effects in non-tumourigenic cells. Mechanistically, LNC2 depletion impaired HR, evidenced by reduced RAD51 foci formation, while having minimal effect on NHEJ. This was accompanied by increased DNA damage and S-phase accumulation, consistent with replication stress. RNA-seq after LNC2 depletion revealed downregulation of DNA repair pathways, including HR and RPA loading, while in vitro mass spectrometry identified HNRNPA2B1 as a LNC2-interacting protein, implicating LNC2 in the regulation of RPA availability and replication fork stability. We propose that LNC2 maintains replication stress tolerance by supporting HR, and that its depletion creates a therapeutically exploitable vulnerability to PARPi. Collectively, these findings establish LNC2 as a key regulator of PARPi response in HGSOC and a promising therapeutic target for improving PARPi inhibitor efficacy.