ArticleThe Journal of cell biology2011
Cdc6 expression represses E-cadherin transcription and activates adjacent replication origins.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 107 citations in OpenAlex.
- The IKKα-regulated microRNA miR-9-5p mediates lung cancer growth and invasiveness via CDH1/Wnt/β-catenin signalling.Cell death discovery · 2026Article
- Review
- CDC6/THBS1 accelerates pancreatic cancer progression via AKT-mediated glycolytic reprogramming.Cell death & disease · 2026Article
- Putrescine functions as a metabolic checkpoint in replication stress-induced senescence.Cellular and molecular life sciences : CMLS · 2025Article
- Exploring the role of exosomal MicroRNAs as potential biomarkers in preeclampsia.Frontiers in immunology · 2024Review
- CDC6, a key replication licensing factor, is overexpressed and confers poor prognosis in diffuse large B-cell lymphoma.BMC cancer · 2023Article
- Review
- A GATA2-CDC6 axis modulates androgen receptor blockade-induced senescence in prostate cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- Prospecting of exosomal-miRNA signatures as prognostic marker for gestational diabetes mellitus and other adverse pregnancy outcomes.Frontiers in endocrinology · 2023Review
- LCAT1 is an oncogenic LncRNA by stabilizing the IGF2BP2-CDC6 axis.Cell death & disease · 2022Article
- An Expanded Interplay Network between NF-κB p65 (RelA) and E2F1 Transcription Factors: Roles in Physiology and Pathology.Cancers · 2022Article
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- Identification of lncRNA/circRNA-miRNA-mRNA ceRNA Network as Biomarkers for Hepatocellular Carcinoma.Frontiers in genetics · 2022Article
- DNA Replication Licensing Factors: Novel Targets for Cancer Therapy via Inhibiting the Stemness of Cancer Cells.International journal of biological sciences · 2022Review
- Article
- Gene expression profile of THZ1-treated nasopharyngeal carcinoma cell lines indicates its involvement in the inhibition of the cell cycle.Translational cancer research · 2021Article
- Article
- Cdc6 as a novel target in cancer: Oncogenic potential, senescence and subcellular localisation.International journal of cancer · 2020Review
- Review
- LSH interacts with and stabilizes GINS4 transcript that promotes tumourigenesis in non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2019Article
Corrections and comments
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Authors and funding
18 authors at 10 institutions in 8 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E-cadherin (CDH1) loss occurs frequently in carcinogenesis, contributing to invasion and metastasis. We observed that mouse and human epithelial cell lines overexpressing the replication licensing factor Cdc6 underwent phenotypic changes with mesenchymal features and loss of E-cadherin. Analysis in various types of human cancer revealed a strong correlation between increased Cdc6 expression and reduced E-cadherin levels. Prompted by these findings, we discovered that Cdc6 repressed CDH1 transcription by binding to the E-boxes of its promoter, leading to dissociation of the chromosomal insulator CTCF, displacement of the histone variant H2A.Z, and promoter heterochromatinization. Mutational analysis identified the Walker B motif and C-terminal region of Cdc6 as essential for CDH1 transcriptional suppression. Strikingly, CTCF displacement resulted in activation of adjacent origins of replication. These data demonstrate that Cdc6 acts as a molecular switch at the E-cadherin locus, linking transcriptional repression to activation of replication, and provide a telling example of how replication licensing factors could usurp alternative programs to fulfill distinct cellular functions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.