ArticleCommunications biology2024
Integrating apaQTL and eQTL analysis identifies a potential causal variant associated with lung adenocarcinoma risk in the Chinese population.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- SERPINE1 Alternative Polyadenylation Influences Gastric Cancer Prognosis via N6-Methyladenosine Modification.Cancer science · 2026Article
- Functions and mechanisms of miR-650 in human diseases.Frontiers in molecular biosciences · 2026Review
- Hyperbaric Oxygen Reverses High-Glucose-Induced Stemness and Radioresistance in Non-Small Cell Lung Cancer Cells.Cancer management and research · 2026Article
- Identifying CTSF and GSTM3 as chemoresistance therapeutic targets in breast cancer through multi-omics MR analysis.iScience · 2025Article
- Integrated genetic and epigenetic analysis identifies that rs939408 affects non-smoking lung adenocarcinoma risk by modulating the DNA methylation of LRRC2.Cell death & disease · 2025Article
- Mendelian randomization study on the association of circulating ketone bodies with lung cancer and respiratory diseases.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Alternative polyadenylation (APA) plays a crucial role in cancer biology. Here, we used data from the 3'aQTL-atlas, GTEx, and the China Nanjing Lung Cancer GWAS database to explore the association between apaQTL/eQTL-SNPs and the risk of lung adenocarcinoma (LUAD). The variant T allele of rs277646 in NIT2 is associated with an increased risk of LUAD (OR = 1.12, P = 0.015), lower PDUI values, and higher NIT2 expression. The 3'RACE experiment showed multiple poly (A) sites in NIT2, with the rs277646-T allele causing preferential use of the proximal poly (A) site, resulting in a shorter 3'UTR transcript. This leads to the loss of the hsa-miR-650 binding site, thereby affecting LUAD malignant phenotypes by regulating the expression level of NIT2. Our findings may provide new insights into understanding and exploring APA events in LUAD carcinogenesis.
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