ArticlePloS one2014
Impact of gene dosage on gene expression, biological processes and survival in cervical cancer: a genome-wide follow-up study.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Pooled it
- A bioinformatics analysis of KIF transcriptomic subtyping reveals prognostic heterogeneity and differential therapeutic responses in cervical cancer.Oncology letters · 2026Article
- Epithelial Cell-Specific Prognostic Signature (FTH1, RIT1, WASL, NDRG2, KIFC3) Stratifies Cervical Cancer Patients and Correlates With Immune Infiltration.Human mutation · 2026Article
- Proteogenomic characterization of molecular and cellular targets for treatment-resistant subtypes in locally advanced cervical cancers.Molecular cancer · 2025Article
- Identification of a disulfidptosis-related genes signature for diagnostic and immune infiltration characteristics in cervical cancer.PloS one · 2025Article
- Downregulation of RhoB Inhibits Cervical Cancer Progression and Enhances Cisplatin Sensitivity.Genes · 2024Article
- Commentary: Immune cell infiltration and prognostic index in cervical cancer: insights from metabolism-related differential genes.Frontiers in immunology · 2024Article
- Comprehensive analysis of autophagy associated genes and immune infiltrates in cervical cancer.Iranian journal of basic medical sciences · 2024Article
- Programmed cell death-index (PCDi) as a prognostic biomarker and predictor of drug sensitivity in cervical cancer: a machine learning-based analysis of mRNA signatures.Journal of Cancer · 2024Article
- Article
- Article
- Construction of a prognostic model based on eight ubiquitination-related genesFrontiers in genetics · 2023Article
- Drug repositioningFrontiers in oncology · 2023Article
- Genomic heterogeneity in pancreatic cancer organoids and its stability with culture.NPJ genomic medicine · 2022Article
- Gene signatures, immune infiltration, and drug sensitivity based on a comprehensive analysis of m6a RNA methylation regulators in cervical cancer.Journal of translational medicine · 2022Article
- ATM Pathway Is Essential for HPV-Positive Human Cervical Cancer-Derived Cell Lines Viability and Proliferation.Pathogens (Basel, Switzerland) · 2022Article
- A novel gene signature associated with poor response to chemoradiotherapy in patients with locally advanced cervical cancer.Journal of gynecologic oncology · 2022Article
- Functional New Transcription Factors (TFs) Associated with Cervical Cancer.Journal of healthcare engineering · 2022Article
- Repositioning of Anti-Inflammatory Drugs for the Treatment of Cervical Cancer Sub-Types.Frontiers in pharmacology · 2022Article
- Integrative meta-analysis of gene expression profiles identifies FEN1 and ENDOU as potential diagnostic biomarkers for cervical squamous cell carcinoma.Oncology letters · 2021Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the role of tumor copy number (CN)-altered genome (CN-AG) in the carcinogenesis of cervical cancer (CC), especially its effect on gene expression, biological processes, and patient survival. Fifty-nine human papillomavirus 16 (HPV16)-positive CCs were investigated with microarrays-31 for mapping CN-AG and 55 for global gene expression, with 27 CCs in common. Five-year survival was investigated in 55 patients. Deletions and amplifications >2.5 Mb were defined as CN alterations. The %CN-AG varied from 0 to 32.2% (mean = 8.1±8.9). Tumors were classified as low (mean = 0.5±0.6, n = 11), medium (mean = 5.4±2.4, n = 10), or high (mean = 19.2±6.6, n = 10) CN. The highest %CN-AG was found in 3q, which contributed an average of 55% of all CN alterations. Genome-wide, only 5.3% of CN-altered genes were deregulated directly by gene dosage. In contrast, the rate in fully duplicated 3q was twice as high. Amplification of 3q explained 23.2% of deregulated genes in whole tumors (r2 = 0.232, p = 0.006; analysis of variance), including genes located in 3q and other chromosomes. A total of 862 genes were deregulated exclusively in high-CN tumors, but only 22.9% were CN altered. This suggests that the remaining genes are not deregulated directly by gene dosage, but by mechanisms induced in trans by CN-altered genes. Anaphase-promoting complex/cyclosome (APC/C)-dependent proteasome proteolysis, glycolysis, and apoptosis were upregulated, whereas cell adhesion and angiogenesis were downregulated exclusively in high-CN tumors. The high %CN-AG and upregulated gene expression profile of APC/C-dependent proteasome proteolysis were associated with poor patient survival (p<0.05, log-rank test). Along with glycolysis, they were linearly associated with FIGO stage (r>0.38, p<0.01, Spearman test). Therefore, inhibition of APC/C-dependent proteasome proteolysis and glycolysis could be useful for CC treatment. However, whether they are indispensable for tumor growth remains to be demonstrated.
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