ArticleNeoplasia (New York, N.Y.)2013
A novel mechanism for CTCF in the epigenetic regulation of Bax in breast cancer cells.
Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- miR-215-5p Suppresses Proliferation/Cell-Cycle Progression and Promotes Apoptosis via Targeting CTCF in Goat Mammary Epithelial Cells.Animals : an open access journal from MDPI · 2026Article
- Functional and Regulatory Effects of Factor V Leiden and Factor V rs6028 in Breast Cancer.Genes · 2025Article
- The Regulatory Role of CTCF in IL6 Gene Transcription Assessed in Breast Cancer Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Association of mutation and expression of the brother of the regulator of imprinted sites (BORIS) gene with breast cancer progression.Oncotarget · 2023Article
- Mechanisms of TP53 Pathway Inactivation in Embryonic and Somatic Cells-Relevance for Understanding (Germ Cell) Tumorigenesis.International journal of molecular sciences · 2021Review
- Genomic retargeting of p53 and CTCF is associated with transcriptional changes during oncogenic HRas-induced transformation.Communications biology · 2020Article
- Association of mutation and low expression of theSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020Article
- Review
- Downregulation of p53 by Insufficient CTCF in CD4Frontiers in immunology · 2020Article
- The X-linked tumor suppressor TSPX downregulates cancer-drivers/oncogenes in prostate cancer in a C-terminal acidic domain dependent manner.Oncotarget · 2019Article
- Article
- Discovering a binary CTCF code with a little help from BORIS.Nucleus (Austin, Tex.) · 2018Review
- Identification and validation of colorectal neoplasia-specific methylation biomarkers based on CTCF-binding sites.Oncotarget · 2017Article
- The CCCTC-binding factor (CTCF)-forkhead box protein M1 axis regulates tumour growth and metastasis in hepatocellular carcinoma.The Journal of pathology · 2017Article
- CCCTC-binding factor inhibits breast cancer cell proliferation and metastasis via inactivation of the nuclear factor-kappaB pathway.Oncotarget · 2017Article
- Functional roles of CTCF in breast cancer.BMB reports · 2017Article
- CTCF interacts with the lytic HSV-1 genome to promote viral transcription.Scientific reports · 2017Article
- Depletion of CTCF in Breast Cancer Cells Selectively Induces Cancer Cell Death via p53.Journal of Cancer · 2017Article
- The dual specificity phosphatase 2 gene is hypermethylated in human cancer and regulated by epigenetic mechanisms.BMC cancer · 2016Article
- Epigenetic silencing of the XAF1 gene is mediated by the loss of CTCF binding.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
We previously reported the association of elevated levels of the multifunctional transcription factor, CCCTC binding factor (CTCF), in breast cancer cells with the specific anti-apoptotic function of CTCF. To understand the molecular mechanisms of this phenomenon, we investigated regulation of the human Bax gene by CTCF in breast and non-breast cells. Two CTCF binding sites (CTSs) within the Bax promoter were identified. In all cells, breast and non-breast, active histone modifications were present at these CTSs, DNA harboring this region was unmethylated, and levels of Bax mRNA and protein were similar. Nevertheless, up-regulation of Bax mRNA and protein and apoptotic cell death were observed only in breast cancer cells depleted of CTCF. We proposed that increased CTCF binding to the Bax promoter in breast cancer cells, by comparison with non-breast cells, may be mechanistically linked to the specific apoptotic phenotype in CTCF-depleted breast cancer cells. In this study, we show that CTCF binding was enriched at the Bax CTSs in breast cancer cells and tumors; in contrast, binding of other transcription factors (SP1, WT1, EGR1, and c-Myc) was generally increased in non-breast cells and normal breast tissues. Our findings suggest a novel mechanism for CTCF in the epigenetic regulation of Bax in breast cancer cells, whereby elevated levels of CTCF support preferential binding of CTCF to the Bax CTSs. In this context, CTCF functions as a transcriptional repressor counteracting influences of positive regulatory factors; depletion of breast cancer cells from CTCF therefore results in the activation of Bax and apoptosis.
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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.