ArticleOncology letters2021
Nuclear factor I/B mediates epithelial-mesenchymal transition in human melanoma cells through ZEB1.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Molecular basis of NFIB-mediated regulation of oncogenic transcription.Nucleic acids research · 2025Article
- Suppression of malignant melanoma by knocking down growth differentiation factor-15 via inhibiting PTEN/PI3K/AKT signaling pathway.Journal of Cancer · 2024Article
- MiR-326-mediated overexpression of NFIB offsets TGF-β induced epithelial to mesenchymal transition and reverses lung fibrosis.Cellular and molecular life sciences : CMLS · 2023Article
- CircIFFO1 suppresses tumor growth and metastasis of cutaneous squamous cell carcinoma by targeting the miR-424-5p/NFIB axis.Archives of dermatological research · 2023Article
- miR-940 is a new biomarker with tumor diagnostic and prognostic value.Molecular therapy. Nucleic acids · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The relationship between nuclear factor I/B (NFIB) and cancer attracts growing research interest. NFIB has diverse and specific roles in tumor progression and invasion. However, the potential effects and functions of this transcription factor in melanoma remain unclear. The present study sought to determine the distinguishing properties of NFIB in melanoma cells. Immunohistochemical examination of the tissues of 15 patients with melanoma indicated that the expression of NFIB was high in melanoma specimens, compared with the benign nevus and normal skin specimens. In addition, the relationship between high NFIB expression and low overall survival rate was assessed. Functional studies demonstrated that NFIB enhanced the malignancy of melanoma, including proliferation, migration and invasion. In addition, NFIB silencing in A375 and A875 cell lines inhibited the process of epithelial-mesenchymal transition (EMT), upregulated E-cadherin and zona occludens-1, but suppressed N-cadherin and vimentin expression. These findings may suggest a new function of NFIB in promoting the migration and invasion of melanoma cells. Therefore, the present study further evaluated the association between NFIB and zinc finger protein E-box binding homeobox-1 (ZEB1) in melanoma. Mechanistic experiments revealed that NFIB exerted its roles during EMT by regulating ZEB1. Overall, the present data indicates that NFIB promotes the malignancy of melanoma, particularly EMT, by modulating the ZEB1 axis, such as ZEB2, ATM and CHK1, which may represent a potential molecular therapeutic target in melanoma.
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Registered trials
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