ArticleMolecular cancer research : MCR2016
Transcription Factor KLF5 Binds a Cyclin E1 Polymorphic Intronic Enhancer to Confer Increased Bladder Cancer Risk.
Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- The landscape of GWAS validation; systematic review identifying 309 validated non-coding variants across 130 human diseases.BMC medical genomics · 2022Pooled it
- Comprehensive Mendelian randomization and colocalization analysis of plasma proteomics to identify new therapeutic targets for bladder cancer.Journal of Cancer · 2025Article
- Abrogation of KLF5 sensitizesActa biochimica et biophysica Sinica · 2024Article
- A Functional Variant Alters the Binding ofAnimals : an open access journal from MDPI · 2023Article
- Computational Assessment of the Expression-modulating Potential for Non-coding Variants.Genomics, proteomics & bioinformatics · 2023Article
- Diet quality, common genetic polymorphisms, and bladder cancer risk in a New England population-based study.European journal of nutrition · 2022Article
- Systems Drug Design for Muscle Invasive Bladder Cancer and Advanced Bladder Cancer by Genome-Wide Microarray Data and Deep Learning Method with Drug Design Specifications.International journal of molecular sciences · 2022Article
- Secreted miR-153 Controls Proliferation and Invasion of Higher Gleason Score Prostate Cancer.International journal of molecular sciences · 2022Article
- Article
- Expression and Prognosis Value of the KLF Family Members in Colorectal Cancer.Journal of oncology · 2022Article
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
- Krüppel-like factor 5 is upregulated and induces cell proliferation in endometrial cancer.Oncology letters · 2021Article
- Polymorphisms of KLF3 gene coding region and identification of their functionality for abdominal fat in chickens.Veterinary medicine and science · 2021Article
- KLF5-Modulated lncRNA NEAT1 Contributes to Tumorigenesis by Acting as a Scaffold for BRG1 to Silence GADD45A in Gastric Cancer.Molecular therapy. Nucleic acids · 2020Article
- Article
- Nurr1 performs its anti-inflammatory function by regulating RasGRP1 expression in neuro-inflammation.Scientific reports · 2020Article
- ML264 inhibits osteosarcoma growth and metastasis via inhibition of JAK2/STAT3 and WNT/β-catenin signalling pathways.Journal of cellular and molecular medicine · 2020Article
- KLF5 Is Crucial for Androgen-AR Signaling to Transactivate Genes and Promote Cell Proliferation in Prostate Cancer Cells.Cancers · 2020Article
- Network analysis ofCancer cell international · 2020Article
- Genetic variant of MAML2 in the NOTCH signaling pathway and the risk of bladder cancer: A STROBE-compliant study.Medicine · 2020Observational
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3 authors at 1 institution in 1 country.
Funding
Abstract
It is well established that environmental toxins, such as exposure to arsenic, are risk factors in the development of urinary bladder cancer, yet recent genome-wide association studies (GWAS) provide compelling evidence that there is a strong genetic component associated with disease predisposition. A single-nucleotide polymorphism (SNP), rs8102137, was identified on chromosome 19q12, residing 6 kb upstream of the important cell-cycle regulator and proto-oncogene, Cyclin E1 (CCNE1). However, the functional role of this variant in bladder cancer predisposition has been unclear because it lies within a non-coding region of the genome. Here, it is demonstrated that bladder cancer cells heterozygous for this SNP exhibit biased allelic expression of CCNE1 with 1.5-fold more transcription occurring from the risk allele. Furthermore, using chromatin immunoprecipitation assays, a novel enhancer element was identified within the first intron of CCNE1 that binds Kruppel-like Factor 5 (KLF5), a known transcriptional activator in bladder cancer. Moreover, the data reveal that the presence of rs200996365, a SNP in high-linkage disequilibrium with rs8102137 residing in the center of a KLF5 motif, alters KLF5 binding to this genomic region. Through luciferase assays and CRISPR-Cas9 genome editing, a novel polymorphic intronic regulatory element controlling CCNE1 transcription is characterized. These studies uncover how a cancer-associated polymorphism mechanistically contributes to an increased predisposition for bladder cancer development. IMPLICATIONS: A polymorphic KLF5 binding site near the CCNE1 gene explains genetic risk identified through GWAS. Mol Cancer Res; 14(11); 1078-86. ©2016 AACR.
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