Reduced ribosomal RNA expression and unchanged ribosomal DNA promoter methylation in oral squamous cell carcinoma.
Adult
Carcinoma, Squamous Cell
/ genetics
Cell Line, Tumor
CpG Islands
/ genetics
DNA Methylation
/ genetics
DNA, Ribosomal
/ genetics
Female
Gene Expression
/ genetics
Gene Expression Regulation, Neoplastic
/ genetics
Humans
Male
Middle Aged
Mouth Neoplasms
/ genetics
Promoter Regions, Genetic
/ genetics
RNA, Ribosomal
/ genetics
Transcriptome
/ genetics
DNA methylation
epigenetics
oral squamous cell carcinoma
rDNA
rRNA
Journal
Molecular genetics & genomic medicine
ISSN: 2324-9269
Titre abrégé: Mol Genet Genomic Med
Pays: United States
ID NLM: 101603758
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
received:
01
03
2019
revised:
07
05
2019
accepted:
17
05
2019
pubmed:
7
6
2019
medline:
16
7
2020
entrez:
7
6
2019
Statut:
ppublish
Résumé
Ribosomal RNA (rRNA) consists of four non-coding RNAs, the 28S, 5.8S, 18S, and 5S rRNA. Abnormal expression of rRNA has been found in multiple tumors, and the methylation of rDNA promoter may affect rRNA expression as an epigenetic regulatory mechanism. Oral squamous cell carcinoma (OSCC) is a kind of aggressive tumors which occurs in multiple sites in oral cavity. rRNA expression and the methylation of rDNA promoter in modulating rRNA expression in OSCC maintain unclear. This study aims to investigate the rRNA expression, the methylation status within rDNA promoter, and the underlying mechanism of methylation in regulating rRNA expression in OSCC. Twelve primary OSCC and matched normal tissue samples were collected from patients with OSCC. Quantitative real-time PCR was used to evaluate the rRNA level. HpaII/MspI digestion and bisulfite sequencing were used to investigate the methylation status of rDNA promoter. Ribosomal RNA levels were suppressed in OSCC as compared with matched normal tissues. HpaII/MspI digestion and bisulfite sequencing showed no significant differences for the methylation of rDNA promoter between the tumor and matched normal tissues. The methylation in rDNA promoter could not explain for the suppressed rRNA expression in OSCC tissues.
Sections du résumé
BACKGROUND
Ribosomal RNA (rRNA) consists of four non-coding RNAs, the 28S, 5.8S, 18S, and 5S rRNA. Abnormal expression of rRNA has been found in multiple tumors, and the methylation of rDNA promoter may affect rRNA expression as an epigenetic regulatory mechanism. Oral squamous cell carcinoma (OSCC) is a kind of aggressive tumors which occurs in multiple sites in oral cavity. rRNA expression and the methylation of rDNA promoter in modulating rRNA expression in OSCC maintain unclear. This study aims to investigate the rRNA expression, the methylation status within rDNA promoter, and the underlying mechanism of methylation in regulating rRNA expression in OSCC.
METHODS
Twelve primary OSCC and matched normal tissue samples were collected from patients with OSCC. Quantitative real-time PCR was used to evaluate the rRNA level. HpaII/MspI digestion and bisulfite sequencing were used to investigate the methylation status of rDNA promoter.
RESULTS
Ribosomal RNA levels were suppressed in OSCC as compared with matched normal tissues. HpaII/MspI digestion and bisulfite sequencing showed no significant differences for the methylation of rDNA promoter between the tumor and matched normal tissues.
CONCLUSION
The methylation in rDNA promoter could not explain for the suppressed rRNA expression in OSCC tissues.
Identifiants
pubmed: 31169368
doi: 10.1002/mgg3.783
pmc: PMC6625366
doi:
Substances chimiques
DNA, Ribosomal
0
RNA, Ribosomal
0
Banques de données
GENBANK
['U13369.1']
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e00783Informations de copyright
© 2019 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc.
Références
Nat Rev Mol Cell Biol. 2003 Aug;4(8):641-9
pubmed: 12923526
Hum Mol Genet. 2002 Oct 1;11(20):2479-88
pubmed: 12351584
Nat Rev Cancer. 2007 Aug;7(8):599-612
pubmed: 17646865
Genes Dev. 1997 Aug 15;11(16):2124-36
pubmed: 9284051
PLoS Genet. 2017 Sep 7;13(9):e1006994
pubmed: 28880866
Nat Rev Cancer. 2011 Jan;11(1):9-22
pubmed: 21160525
Genes Dev. 2003 Jul 15;17(14):1691-702
pubmed: 12865296
Cell Cycle. 2009 Jul 1;8(13):2101-9
pubmed: 19502796
CA Cancer J Clin. 2015 Mar;65(2):87-108
pubmed: 25651787
Oncotarget. 2016 Oct 25;7(43):69579-69591
pubmed: 27602958
Nat Rev Cancer. 2005 Feb;5(2):127-35
pubmed: 15685196
Nat Rev Genet. 2002 Jun;3(6):415-28
pubmed: 12042769
Head Neck. 2008 Jan;30(1):75-84
pubmed: 17694557
Pediatr Res. 1973 Jan;7(1):5-12
pubmed: 4687000
J Cell Biochem. 1999;Suppl 32-33:41-50
pubmed: 10629102
Hum Mol Genet. 2001 Apr;10(7):687-92
pubmed: 11257100
J Cell Physiol. 2015 Jun;230(6):1181-8
pubmed: 25336383
Cancer Res. 2012 Aug 1;72(15):3753-63
pubmed: 22659451
Mol Genet Genomic Med. 2019 Jul;7(7):e00783
pubmed: 31169368
Nat Rev Genet. 2000 Oct;1(1):11-9
pubmed: 11262868
Oncol Rep. 2015 Jun;33(6):3131-45
pubmed: 25962577
Int J Clin Oncol. 2016 Oct;21(5):883-889
pubmed: 27000845
Oncogene. 2012 Mar 8;31(10):1254-63
pubmed: 21822302
Epigenetics. 2010 Apr;5(3):200-5
pubmed: 20305389
Cancer Metastasis Rev. 2007 Dec;26(3-4):645-62
pubmed: 17768600
J Biol Chem. 2004 Feb 20;279(8):6783-93
pubmed: 14610093
Oncogene. 2017 Nov 2;36(44):6109-6118
pubmed: 28692053
Blood. 2012 Dec 6;120(24):4812-8
pubmed: 23071274
Annu Rev Pharmacol Toxicol. 2010;50:131-56
pubmed: 20055700
PLoS One. 2016 Oct 3;11(10):e0163340
pubmed: 27695092
Trends Biochem Sci. 1999 Nov;24(11):437-40
pubmed: 10542411
Ear Nose Throat J. 2006 Feb;85(2):74
pubmed: 16579185
Nat Rev Cancer. 2003 Mar;3(3):179-92
pubmed: 12612653