ArticlePloS one2015
Different Effects of BORIS/CTCFL on Stemness Gene Expression, Sphere Formation and Cell Survival in Epithelial Cancer Stem Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Transcriptome signatures for the identification of bevacizumab responders in ovarian cancer.Genome medicine · 2026Article
- Mechanism of miR-98-5p in gastric cancer cell proliferation, migration, and invasion through the USP44/CTCFL axis.Toxicology research · 2024Article
- Retraction Note: The BET inhibitor I-BET762 inhibits pancreatic ductal adenocarcinoma cell proliferation and enhances the therapeutic effect of gemcitabine.Scientific reports · 2023Article
- A Therapeutic Vaccine Targeting Rat BORIS (CTCFL) for the Treatment of Rat Breast Cancer Tumors.International journal of molecular sciences · 2023Article
- Inhibitory Effects of Ursolic Acid on the Stemness and Progression of Human Breast Cancer Cells by Modulating Argonaute-2.International journal of molecular sciences · 2022Article
- CTCFL regulates the PI3K-Akt pathway and it is a target for personalized ovarian cancer therapy.NPJ systems biology and applications · 2022Article
- Immunoprotective effect of an in silico designed multiepitope cancer vaccine with BORIS cancer-testis antigen target in a murine mammary carcinoma model.Scientific reports · 2021Article
- Telomerase inhibition decreases esophageal squamous carcinoma cell migration and invasion.Oncology letters · 2020Article
- Recent Advances in Liver Cancer Stem Cells: Non-coding RNAs, Oncogenes and Oncoproteins.Frontiers in cell and developmental biology · 2020Review
- Article
- The epigenetic factor BORIS (CTCFL) controls the androgen receptor regulatory network in ovarian cancer.Oncogenesis · 2019Article
- Targeting CTCFL/BORIS for the immunotherapy of cancer.Cancer immunology, immunotherapy : CII · 2018Review
- Choice of binding sites for CTCFL compared to CTCF is driven by chromatin and by sequence preference.Nucleic acids research · 2018Article
- Distinct DNA Methylation Profiles in Ovarian Tumors: Opportunities for Novel Biomarkers.International journal of molecular sciences · 2018Article
- BORIS: a key regulator of cancer stemness.Cancer cell international · 2018Review
- Immunophenotypic characterization of sphere-forming cells derived from the human renal cell carcinoma cell line 786-O.American journal of translational research · 2018Article
- Article
- Observational
- Brother of Regulator of Imprinted Sites (BORIS) suppresses apoptosis in colorectal cancer.Scientific reports · 2017Article
- The cancer-associated CTCFL/BORIS protein targets multiple classes of genomic repeats, with a distinct binding and functional preference for humanoid-specific SVA transposable elements.Epigenetics & chromatin · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells are cancer cells characterized by stem cell properties and represent a small population of tumor cells that drives tumor development, progression, metastasis and drug resistance. To date, the molecular mechanisms that generate and regulate cancer stem cells are not well defined. BORIS (Brother of Regulator of Imprinted Sites) or CTCFL (CTCF-like) is a DNA-binding protein that is expressed in normal tissues only in germ cells and is re-activated in tumors. Recent evidences have highlighted the correlation of BORIS/CTCFL expression with poor overall survival of different cancer patients. We have previously shown an association of BORIS-expressing cells with stemness gene expression in embryonic cancer cells. Here, we studied the role of BORIS in epithelial tumor cells. Using BORIS-molecular beacon that was already validated, we were able to show the presence of BORIS mRNA in cancer stem cell-enriched populations (side population and spheres) of cervical, colon and breast tumor cells. BORIS silencing studies showed a decrease of sphere formation capacity in breast and colon tumor cells. Importantly, BORIS-silencing led to down-regulation of hTERT, stem cell (NANOG, OCT4, SOX2 and BMI1) and cancer stem cell markers (ABCG2, CD44 and ALDH1) genes. Conversely, BORIS-induction led to up-regulation of the same genes. These phenotypes were observed in cervical, colon and invasive breast tumor cells. However, a completely different behavior was observed in the non-invasive breast tumor cells (MCF7). Indeed, these cells acquired an epithelial mesenchymal transition phenotype after BORIS silencing. Our results demonstrate that BORIS is associated with cancer stem cell-enriched populations of several epithelial tumor cells and the different phenotypes depend on the origin of tumor cells.
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