ArticleCancer research2009
Haplotype and cell proliferation analyses of candidate lung cancer susceptibility genes on chromosome 15q24-25.1.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Pooled it
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- PSMA4 as a Druggable Target in Hidradenitis Suppurativa: Evidence From Mendelian Randomization and Single-Cell Transcriptomics.Mediators of inflammation · 2026Article
- From locus to gene: causal inference and experimental validation prioritize PSMA4 as a candidate target in lung adenocarcinoma.American journal of cancer research · 2026Article
- Genetic architecture of RNA editing, splicing and gene expression in schizophrenia.Human molecular genetics · 2025Article
- Using Mendelian randomization provides genetic insights into potential targets for sepsis treatment.Scientific reports · 2024Article
- Single-cell and transcriptomic analyses reveal the influence of diabetes on ovarian cancer.BMC genomics · 2024Article
- Therapeutic targets for lung cancer: genome-wide Mendelian randomization and colocalization analyses.Frontiers in pharmacology · 2024Article
- Functional studies of lung cancer GWAS beyond association.Human molecular genetics · 2022Review
- Upregulated Proteasome Subunits in COVID-19 Patients: A Link with Hypoxemia, Lymphopenia and Inflammation.Biomolecules · 2022Article
- Identification of Prognostic and Chemopredictive microRNAs for Non-Small-Cell Lung Cancer by Integrating SEER-Medicare Data.International journal of molecular sciences · 2021Article
- NR2F1-AS1 Promotes Pancreatic Ductal Adenocarcinoma Progression Through Competing Endogenous RNA Regulatory Network Constructed by Sponging miRNA-146a-5p/miRNA-877-5p.Frontiers in cell and developmental biology · 2021Article
- Identifying Putative Susceptibility Genes and Evaluating Their Associations with Somatic Mutations in Human Cancers.American journal of human genetics · 2019Article
- Comparison of different functional prediction scores using a gene-based permutation model for identifying cancer driver genes.BMC medical genomics · 2019Article
- Genetic modifiers of radon-induced lung cancer risk: a genome-wide interaction study in former uranium miners.International archives of occupational and environmental health · 2018Article
- A Decade of GWAS Results in Lung Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018Review
- Weak sharing of genetic association signals in three lung cancer subtypes: evidence at the SNP, gene, regulation, and pathway levels.Genome medicine · 2018Article
- Article
- The transcription levels and prognostic values of seven proteasome alpha subunits in human cancers.Oncotarget · 2017Article
- Novel Mutations of the CHRNA3 Gene in Non-Small Cell Lung Cancer in an Iranian PopulationAsian Pacific journal of cancer prevention : APJCP · 2017Article
Corrections and comments
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Authors and funding
24 authors at 11 institutions in 1 country.
Funding
Abstract
Recent genome-wide association studies have linked the chromosome 15q24-25.1 locus to nicotine addiction and lung cancer susceptibility. To refine the 15q24-25.1 locus, we performed a haplotype-based association analysis of 194 familial lung cases and 219 cancer-free controls from the Genetic Epidemiology of Lung Cancer Consortium (GELCC) collection, and used proliferation and apoptosis analyses to determine which gene(s) in the 15q24-25.1 locus mediates effects on lung cancer cell growth in vitro. We identified two distinct subregions, hapL (P = 3.20 x 10(-6)) and hapN (P = 1.51 x 10(-6)), which were significantly associated with familial lung cancer. hapL encompasses IREB2, LOC123688, and PSMA4, and hapN encompasses the three nicotinic acetylcholine receptor subunit genes CHRNA5, CHRNA3, and CHRNB4. Examination of the genes around hapL revealed that PSMA4 plays a role in promoting cancer cell proliferation. PSMA4 mRNA levels were increased in lung tumors compared with normal lung tissues. Down-regulation of PSMA4 expression decreased proteasome activity and induced apoptosis. Proteasome dysfunction leads to many diseases including cancer, and drugs that inhibit proteasome activity show promise as a form of cancer treatment. Genes around hapN were also investigated, but did not show any direct effect on lung cancer cell proliferation. We concluded that PSMA4 is a strong candidate mediator of lung cancer cell growth, and may directly affect lung cancer susceptibility through its modulation of cell proliferation and apoptosis.
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