ArticleMolecular cancer2008
Integrative genomics analysis of chromosome 5p gain in cervical cancer reveals target over-expressed genes, including Drosha.
Article in Molecular cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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65 citing papers in PubMed, 122 citations in OpenAlex.
- Trial
- The Hidden Layer of MicroRNA Regulation in Gynecologic Cancers: IsomiRs, Arm Switching, and RNA Epitranscriptomic Modifications.International journal of molecular sciences · 2026Review
- Key imidazolyl groups that induce phenylalanine flipping enhance the efficacy of oral BRD9 inhibitors for AML treatment.Acta pharmaceutica Sinica. B · 2025Article
- Article
- Risk of Cervical Carcinoma After Unfavorable Behavior and High Genetic Risk in the UK Biobank: A Prospective Nested Case-Control Study.Biomedicines · 2025Article
- Identification and Development of BRD9 Chemical Probes.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Characterization of tumor microenvironment and tumor immunology based on the double-stranded RNA-binding protein related genes in cervical cancer.Journal of translational medicine · 2023Article
- Chemically induced degradation of epigenetic targets.Chemical Society reviews · 2023Review
- Adaptation to spindle assembly checkpoint inhibition through the selection of specific aneuploidies.Genes & development · 2023Article
- PAIP1 is a novel oncogene in human hepatocellular carcinoma.Discover oncology · 2022Article
- The Dysregulation of MicroRNAs in the Development of Cervical Pre-Cancer-An Update.International journal of molecular sciences · 2022Review
- Effect of PAIP1 on the metastatic potential and prognostic significance in oral squamous cell carcinoma.International journal of oral science · 2022Article
- Murine Oncostatin M Has Opposing Effects on the Proliferation of OP9 Bone Marrow Stromal Cells and NIH/3T3 Fibroblasts Signaling through the OSMR.International journal of molecular sciences · 2021Article
- Review
- BRD9 controls the oxytocin signaling pathway in gastric cancer via CANA2D4, CALML6, GNAO1, and KCNJ5.Translational cancer research · 2020Article
- Genome-wide somatic copy number alteration analysis and database construction for cervical cancer.Molecular genetics and genomics : MGG · 2020Article
- Targeting BRD9 for Cancer Treatment: A New Strategy.OncoTargets and therapy · 2020Review
- Article
- Paip1 Indicated Poor Prognosis in Cervical Cancer and Promoted Cervical Carcinogenesis.Cancer research and treatment · 2019Article
- Paired Box-1 (PAX1) Activates Multiple Phosphatases and Inhibits Kinase Cascades in Cervical Cancer.Scientific reports · 2019Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundCopy number gains and amplifications are characteristic feature of cervical cancer (CC) genomes for which the underlying mechanisms are unclear. These changes may possess oncogenic properties by deregulating tumor-related genes. Gain of short arm of chromosome 5 (5p) is the most frequent karyotypic change in CC.
methodsTo examine the role of 5p gain, we performed a combination of single nucleotide polymorphism (SNP) array, fluorescence in situ hybridization (FISH), and gene expression analyses on invasive cancer and in various stages of CC progression.
resultsThe SNP and FISH analyses revealed copy number increase (CNI) of 5p in 63% of invasive CC, which arises at later stages of precancerous lesions in CC development. We integrated chromosome 5 genomic copy number and gene expression data to identify key target over expressed genes as a consequence of 5p gain. One of the candidates identified was Drosha (RNASEN), a gene that is required in the first step of microRNA (miRNA) processing in the nucleus. Other 5p genes identified as targets of CNI play a role in DNA repair and cell cycle regulation (BASP1, TARS, PAIP1, BRD9, RAD1, SKP2, and POLS), signal transduction (OSMR), and mitochondrial oxidative phosphorylation (NNT, SDHA, and NDUFS6), suggesting that disruption of pathways involving these genes may contribute to CC progression.
conclusionTaken together, we demonstrate the power of integrating genomics data with expression data in deciphering tumor-related targets of CNI. Identification of 5p gene targets in CC denotes an important step towards biomarker development and forms a framework for testing as molecular therapeutic targets.
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