ArticleCell death discovery2020
BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cells.
Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 48 citations in OpenAlex.
- Loss of miR-122 promotes cell migration and poor prognosis in triple-negative breast cancer treated by neoadjuvant chemotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Chromatin architecture and physical constriction cooperate in phenotype switching and cancer cell dissemination.bioRxiv : the preprint server for biology · 2026Article
- Article
- Patient-specific gene co-expression networks reveal novel subtypes and predictive biomarkers in lung adenocarcinoma.NPJ systems biology and applications · 2025Article
- BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.Genome biology · 2024Article
- Review
- Characterization of molecular subtypes based on chromatin regulators and identification of the role of NPAS2 in lung adenocarcinoma.Clinical epigenetics · 2023Article
- Molecular characterization of renal cell carcinoma tumors from a phase III anti-angiogenic adjuvant therapy trial.Nature communications · 2022Article
- ROR2, a driver of "phenotype switching" in melanoma?Cancer cell international · 2022Article
- Tumor-matrix interaction induces phenotypic switching in liver cancer cells.Hepatology international · 2022Article
- Review
- An H3K4me3 reader, BAP18 as an adaptor of COMPASS-like core subunits co-activates ERα action and associates with the sensitivity of antiestrogen in breast cancer.Nucleic acids research · 2020Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma is among the most aggressive cancers due to its tendency to metastasize early. Phenotype switching between a proliferative and an invasive state has been suggested as a critical process for metastasis, though the mechanisms that regulate state transitions are complex and remain poorly understood. Brother of Regulator of Imprinted Sites (BORIS), also known as CCCTC binding factor-Like (CTCFL), is a transcriptional modulator that becomes aberrantly expressed in melanoma. Yet, the role of BORIS in melanoma remains elusive. Here, we show that BORIS is involved in melanoma phenotype switching. Genetic modification of BORIS expression in melanoma cells combined with whole-transcriptome analysis indicated that BORIS expression contributes to an invasion-associated transcriptome. In line with these findings, inducible BORIS overexpression in melanoma cells reduced proliferation and increased migration and invasion, demonstrating that the transcriptional switch is accompanied by a phenotypic switch. Mechanistically, we reveal that BORIS binds near the promoter of transforming growth factor-beta 1 (
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