Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Objective: To investigate the regulatory role of stemness factor BMI1 in epithelial-mesenchymal transition (EMT) and metastasis of tongue squamous cell carcinoma (TSCC) METHODS: Clinical and mouse TSCC specimens were analyzed for BMI1/TGF-β1 expression via immunohistochemistry (IHC). In vitro studies used SCC-9 cells with independent knockdown of BMI1 or TGF-β1; Protein levels quantified by RT-qPCR, Western blot, and immunofluorescence. Migration capacity assessed by Transwell and wound healing assays.
Results: BMI1 was significantly upregulated in human and murine TSCC tissues. TGF-β1 knockdown reduced both E-cadherin and N-cadherin expression. BMI1 knockdown increased TGF-β1 expression but induced accumulation of dysfunctional cytoplasmic SMAD complexes. Both knockdowns impaired cell migration.
Conclusions: BMI1 maintains a pro-metastatic partial EMT (pEMT) state in TSCC by regulating TGF-β1. BMI1 knockdown dysregulates TGF-β1/SMAD signaling, trapping cells in a hybrid phenotype with disrupted cadherin balance and suppressed collective migration.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.oraloncology.2025.107603 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
CFTR ion transport deficiency primes the epithelium for partial epithelial-mesenchymal transition in cystic fibrosis.
Front Pharmacol
August 2025
BioISI-Biosystems & Integrative Sciences Institute, Faculty of Sciences, University of Lisboa, Lisboa, Portugal.
Introduction: Cystic fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes a Cl/HCO ion channel located at the apical plasma membrane (PM) of epithelial cells. CFTR dysfunction disrupts epithelial barrier integrity, drives progressive airway remodelling and has been associated with epithelial-to-mesenchymal transition (EMT), a process in which cells lose epithelial properties and acquire mesenchymal characteristics. We previously demonstrated that mutant CFTR directly drives partial EMT, independently of secondary events such as bacterial infection or inflammation.
View Article and Find Full Text PDFEpithelial fusion is mediated by a partial epithelial-mesenchymal transition.
Biol Open
September 2025
National Centre for Biological Sciences, Tata Institute for Fundamental Research, GKVK PO, Bellary Road, Bangalore, 560065, India.
Epithelial fusion is a fundamental morphogenetic process critical for the closure and compartmentalisation of developing organs. While widely studied in systems such as neural tube and palatal closure, the cellular transitions that enable fusion remain poorly understood. Here, we investigate epithelial fusion during chick otic vesicle (OV) closure and identify a transient population of cells at the epithelial interface that mediate this process.
View Article and Find Full Text PDFCorrection: Wnt/ERK/CDK4/6 activation in the partial EMT state coordinates mammary cancer stemness with self-renewal and inhibition of differentiation.
Br J Cancer
September 2025
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA.
Oxidative stress-induced ZEB1 acetylation drives a hybrid epithelial-mesenchymal phenotype and promotes lung metastasis in triple-negative breast cancer.
Redox Biol
August 2025
Tianjin Key Laboratory of Tumour Microenvironment and Neurovascular Regulation, School of Medicine, Nankai University, Tianjin, 300071, PR China. Electronic address:
While epithelial-mesenchymal plasticity (EMP) drives cancer metastasis, its regulation by redox dynamics remains poorly understood. Herein, we identified an oxidative stress-responsive CBP/SIRT1 axis that coordinated ZEB1 acetylation at K1108 to promote lung metastasis in triple-negative breast cancer (TNBC). Mechanistically, the biochemical and functional analyses revealed that the dual-acetyltransferase CBP, through stabilization and autoacetylation by oxidative stress, formed a dynamic partnership with SIRT1 to execute precision lysine modification.
View Article and Find Full Text PDFDisruption of sphingolipid and glycosphingolipid profiles in human bronchial epithelial cells and extracellular vesicles during gradual benzo[a]pyrene-induced epithelial-to-mesenchymal transition.
Environ Res
August 2025
Department of Pharmacology and Toxicology, Veterinary Research Institute, Brno, Czech Republic. Electronic address:
In this study, effects of environmental carcinogen benzo[a]pyrene (BaP) on deregulation of sphingolipid (SL) and glycosphingolipid (GSL) metabolism were studied during BaP-induced transformation of normal human bronchial epithelial HBEC-12KT cells. After 2-weeks of exposure, BaP altered their morphology, while it downregulated sphingosine-1-phosphate (S1P) and upregulated sphingosine, gangliosides, GM3 and Lc3 GSLs. A longer, 8-week exposure to BaP, further increased cell migratory capacity, induced epithelial-to-mesenchymal transition (EMT) markers and EMT-related transcriptional regulators (SNAI1, ZEB1 and ZEB2), and it increased intracellular sphingosine, ceramide-1-phosphate, as well as a series of GSLs (glucosylceramide, lactosylceramide, GM1a, GD3, Lc3 and Gb3).
View Article and Find Full Text PDF