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Epigenetic regulation of the X-linked tumour suppressors BEX1 and LDOC1 in oral squamous cell carcinoma
The Journal of pathology, 2013-07, Vol.230 (3), p.298-309
2013

Details

Autor(en) / Beteiligte
Titel
Epigenetic regulation of the X-linked tumour suppressors BEX1 and LDOC1 in oral squamous cell carcinoma
Ist Teil von
  • The Journal of pathology, 2013-07, Vol.230 (3), p.298-309
Ort / Verlag
Chichester, UK: John Wiley & Sons, Ltd
Erscheinungsjahr
2013
Link zum Volltext
Quelle
Wiley-Blackwell Journals
Beschreibungen/Notizen
  • The strong associations between oral squamous cell carcinoma (OSCC) and dietary habits such as alcohol consumption (A), betel quid chewing (B) and cigarette smoking (C) and its predominance in men have been well documented; however, systemic analysis of OSCC is limited. Our study applied high‐throughput screening methods to identify causative epigenetic targets in a cohort of men with ABC‐associated OSCC. We identified BEX1 and LDOC1 as two epigenetically silenced X‐linked tumour suppressors and demonstrated a functional link between the transcription of BEX1 and LDOC1 and promoter hypermethylation. Methylation of the BEX1 and LDOC1 promoters was associated significantly (p < 0.0001) with OSCC and were detected in 75% (42/56) and 89% (50/56) of the samples, respectively. We observed concordant increases in the methylation of both genes in 71% (40/56) of the tumours, and potent in vitro and in vivo growth inhibitory effects in OSCC cells ectopically expressing BEX1 and/or LDOC1. Restored expression of BEX1 and LDOC1 suppressed the nuclear factor‐κB (NF‐κB) signalling pathway, which is the most frequently hyperactivated signalling pathway in OSCC. This suppression might result from decreased p50 and p65 expression. These findings suggest that silencing of BEX1 and LDOC1 by promoter hypermethylation might represent a critical event in the molecular pathogenesis of OSCC and account for the oncogenic effects of ABC exposure and the male predominance of OSCC occurrence. Microarray data are available in the Gene Expression Omnibus (GEO; http://www.ncbi.nlm.nih.gov/geo/) Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Sprache
Englisch
Identifikatoren
ISSN: 0022-3417
eISSN: 1096-9896
DOI: 10.1002/path.4173
Titel-ID: cdi_proquest_miscellaneous_1448223242
Format
–
Schlagworte
Animals, BEX1, Biomarkers, Tumor - genetics, Biomarkers, Tumor - metabolism, Carcinoma, Squamous Cell - genetics, Carcinoma, Squamous Cell - metabolism, Carcinoma, Squamous Cell - pathology, Cell Line, Chewing, Cohort Studies, DNA Methylation, Down-Regulation, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Gene Silencing, Genes, X-Linked, High-Throughput Screening Assays, Humans, hypermethylation, LDOC1, Male, male predominance, Mice, Mice, SCID, Mouth Neoplasms - genetics, Mouth Neoplasms - metabolism, Mouth Neoplasms - pathology, Nerve Tissue Proteins - genetics, Nerve Tissue Proteins - metabolism, NF-kappa B - genetics, NF-kappa B - metabolism, NF-κB, Nuclear Proteins - genetics, Nuclear Proteins - metabolism, Oligonucleotide Array Sequence Analysis, Promoter Regions, Genetic - genetics, Random Allocation, risk factor exposure, Sex Factors, Signal Transduction, Tumor Suppressor Proteins - genetics, Tumor Suppressor Proteins - metabolism, X-linked tumour suppressor gene

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