ArticleAmerican journal of human genetics2022
Functional analysis of the 1p34.3 risk locus implicates GNL2 in high-grade serous ovarian cancer.
Article in American journal of human genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- GNL2 plays a critical role in avian reovirus p17-mediated host cellular autophagy and promotes viral proliferation.Poultry science · 2026Article
- Multi-omics integration identifies ribosome biogenesis-active macrophage subpopulation and its key gene GNL2 in driving liver hepatocellular carcinoma progression and mechanisms.Cancer cell international · 2026Article
- Characterizing somatic mutations in ovarian cancer germline risk regions.Communications biology · 2025Article
- RBIS regulates ribosome biogenesis to affect progression in lung adenocarcinoma.Journal of translational medicine · 2024Article
- GLN2 as a key biomarker and therapeutic target: evidence from a comprehensive pan-cancer study using molecular, functional, and bioinformatic analyses.Discover oncology · 2024Article
- Oncogenic role of RNA-binding protein GNL2 in glioma: Promotion of tumor development through enhancing protein synthesis.Oncology letters · 2024Article
- Identification of hub genes based on integrated analysis of single-cell and microarray transcriptome in patients with pulmonary arterial hypertension.BMC genomics · 2023Article
- DNALI1 is a prognosis-related biomarker and correlates with immune infiltrates in low grade glioma.Cancer biomarkers : section A of Disease markers · 2023Article
- Role of Leucine-Rich Repeat-Containing G-Protein-Coupled Receptors 4-6 (LGR4-6) in the Ovary and Other Female Reproductive Organs: A Literature Review.Cell transplantationReview
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
The high-grade serous ovarian cancer (HGSOC) risk locus at chromosome 1p34.3 resides within a frequently amplified genomic region signifying the presence of an oncogene. Here, we integrate in silico variant-to-function analysis with functional studies to characterize the oncogenic potential of candidate genes in the 1p34.3 locus. Fine mapping of genome-wide association statistics identified candidate causal SNPs local to H3K27ac-demarcated enhancer regions that exhibit allele-specific binding for CTCF in HGSOC and normal fallopian tube secretory epithelium cells (FTSECs). SNP risk associations colocalized with eQTL for six genes (DNALI1, GNL2, RSPO1, SNIP1, MEAF6, and LINC01137) that are more highly expressed in carriers of the risk allele, and three (DNALI1, GNL2, and RSPO1) were upregulated in HGSOC compared to normal ovarian surface epithelium cells and/or FTSECs. Increased expression of GNL2 and MEAF6 was associated with shorter survival in HGSOC with 1p34.3 amplifications. Despite its activation of β-catenin signaling, RSPO1 overexpression exerted no effects on proliferation or colony formation in our study of ovarian cancer and FTSECs. Instead, GNL2, MEAF6, and SNIP1 silencing impaired in vitro ovarian cancer cell growth. Additionally, GNL2 silencing diminished xenograft tumor formation, whereas overexpression stimulated proliferation and colony formation in FTSECs. GNL2 influences 60S ribosomal subunit maturation and global protein synthesis in ovarian cancer and FTSECs, providing a potential mechanism of how GNL2 upregulation might promote ovarian cancer development and mediate genetic susceptibility of HGSOC.
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