ArticleThe FEBS journal2020
Fusobacterium nucleatum promotes epithelial-mesenchymal transiton through regulation of the lncRNA MIR4435-2HG/miR-296-5p/Akt2/SNAI1 signaling pathway.
Article in The FEBS journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.
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Who cites it
106 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.
- Demystifying the link between periodontitis and oral cancer: a systematic review integrating clinical, pre-clinical, and in vitro data.Cancer metastasis reviews · 2025Pooled it
- LncRNA MIR4435-2HG-mediated succinylation of USF1 promotes its protein stability and induces epithelial-mesenchymal transition in HNSCC.Epigenetics · 2026Article
- lncRNA MIR4435-2HG modulates the malignant progression of glioblastoma through the miR-181d-5p/MALT1/NF-κB signaling pathway.Journal of molecular histology · 2026Article
- Targeting tumor-associated bacteria in digestive system cancers: carcinogenic mechanisms and nano-regulate platform design.Journal of nanobiotechnology · 2026Review
- Review
- Fusobacterium nucleatum in cancer: Interactions with microbiota, tumour colonisation and cancer progression.Clinical and translational medicine · 2026Review
- The Silent Link: Exploring the Impact of Periodontal Diseases on Head and Neck Carcinogenesis.Clinical and experimental dental research · 2026Review
- Fusobacterium nucleatum promotes tumor extravasation and metastasis in head and neck cancer via TLR4/MYB/ESPN axis.Communications biology · 2026Article
- Proteomics of Periodontitis-Associated Bacteria and Its Link to Oral Squamous Cell Carcinoma: A Contemporaneous Review.International dental journal · 2026Review
- A pro-carcinogenic oral microbe internalized by breast cancer cells promotes mammary tumorigenesis.Cell communication and signaling : CCS · 2026Article
- Tumor-infiltrating bacteria disrupt cancer epithelial cell interactions and induce cell-cycle arrest.Cancer cell · 2026Article
- The microbiome-inflammation-immune axis in oral squamous cell carcinoma: from mechanistic insights to therapeutic perspectives.Frontiers in immunology · 2026Review
- The mechanism of lncRNA PVT1 in oral squamous cell carcinoma.Frontiers in oncology · 2026Review
- Targeting the MIR4435-2HG/miR-29c-3p/FSP1 axis overcomes lenvatinib resistance by inducing ferroptosis in hepatocellular carcinoma.Cancer cell international · 2025Article
- Microbial dysbiosis and host-microbe interactions in proliferative verrucous leukoplakia: insights into carcinogenic potential.Archives of microbiology · 2025Review
- Integrated proteomics and metabolomics analysis revealed that macrophage-related signals may be potential biomarkers for oral squamous cell carcinoma.Scientific reports · 2025Article
- Microbial oncogenesis: the impact of Fusobacterium nucleatum on oral cancer pathways.Medical oncology (Northwood, London, England) · 2025Review
- Fisetin Inhibits Periodontal Pathogen-Induced EMT in Oral Squamous Cell Carcinoma via the Wnt/β-Catenin Pathway.Nutrients · 2025Article
- Fusobacterium in the microbiome: from health to disease across the oral-gut axis and beyond.NPJ biofilms and microbiomes · 2025Review
- Cold, Hot, and Lethal-The Tumour Microenvironment and the Immunology of Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2025Review
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fusobacterium nucleatum, an anaerobic oral opportunistic pathogen associated with periodontitis, has been considered to be associated with the development of oral squamous cell carcinoma (OSCC). However, the initial host molecular alterations induced by F. nucleatum infection which may promote predisposition to malignant transformation through epithelial-mesenchymal transition (EMT) have not yet been clarified. In the present study, we monitored the ability of F. nucleatum to induce EMT-associated features, and our results showed that F. nucleatum infection promoted cell migration in either noncancerous human immortalized oral epithelial cells (HIOECs) or the two OSCC cell lines SCC-9 and HSC-4, but did not accelerate cell proliferation or cell cycle progression. Mesenchymal markers, including N-cadherin, Vimentin, and SNAI1, were upregulated, while E-cadherin was decreased and was observed to translocate to the cytoplasm. Furthermore, FadA adhesin and heat-inactivated F. nucleatum were found to cause a similar effect as the viable bacterial cells. The upregulated lncRNA MIR4435-2HG identified by the high-throughput sequencing was demonstrated to negatively regulate the expression of miR-296-5p, which was downregulated in F. nucleatum-infected HIOECs and SCC-9 cells. The binding of MIR4435-2HG and miR-296-5p was validated via a dual-luciferase reporter assay. Additionally, knockdown of MIR4435-2HG with siRNA leads to a decrease in SNAI1 expression, while miR-296-5p could further negatively and indirectly regulate SNAI1 expression via Akt2. Therefore, our study demonstrated that F. nucleatum infection could trigger EMT via lncRNA MIR4435-2HG/miR-296-5p/Akt2/SNAI1 signaling pathway, and EMT process may be a probable link between F. nucleatum infection and initiation of oral epithelial carcinomas.
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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.