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Titolo:
The E-cadherin gene is silenced by CpG methylation in human oral squamous cell carcinomas
Autore:
Nakayama, S; Sasaki, A; Mese, H; Alcalde, RE; Tsuji, T; Matsumura, T;
Indirizzi:
Okayama Univ, Sch Dent, Dept Oral & Maxillofacial Surg 2, Okayama 7008525,Japan Okayama Univ Okayama Japan 7008525 ofacial Surg 2, Okayama 7008525,Japan Univ Washington, Dept Oral & Maxillofacial Surg, Seattle, WA USA Univ Washington Seattle WA USA ral & Maxillofacial Surg, Seattle, WA USA Harvard Univ, Sch Dent Med, Div Oral Pathol, Dept Oral Med & Diagnost Sci,Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Med & Diagnost Sci,Boston, MA 02115 USA
Titolo Testata:
INTERNATIONAL JOURNAL OF CANCER
fascicolo: 5, volume: 93, anno: 2001,
pagine: 667 - 673
SICI:
0020-7136(20010901)93:5<667:TEGISB>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
INVASION-SUPPRESSOR GENE; LYMPH-NODE METASTASIS; BREAST-CANCER; ADHESION MOLECULES; TUMOR HETEROGENEITY; ISLAND METHYLATION; DNA METHYLATION; GASTRIC-CANCER; EXPRESSION; INACTIVATION;
Keywords:
E-cadherin; methylation; invasion and metastasis; human tongue SCC;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Nakayama, S Okayama Univ, Sch Dent, Dept Oral & Maxillofacial Surg 2, 2-5-1 Shikata Cho, Okayama 7008525, Japan Okayama Univ 2-5-1 Shikata Cho Okayama Japan 7008525 5, Japan
Citazione:
S. Nakayama et al., "The E-cadherin gene is silenced by CpG methylation in human oral squamous cell carcinomas", INT J CANC, 93(5), 2001, pp. 667-673

Abstract

Reduction of E-cadherin strongly relates to invasiveness and metastasis invitro. To clarify CpG methylation around the promoter region of the E-cadherin gene in oral squamous cell carcinoma (SCC), we examined the DNA samples of various human SCC cell lines and primary oral SCC tissues by methylation-specific polymerase chain reaction (MSP). CpG methylation of the E-cadherin gene markedly correlated to the reduction of E-cadherin expression in human oral SCC cell lines. In primary oral SCC tissues, only 1 of 5 preserved E-cadherin-expressing tissues was methylated, whereas methylation was found in 17 (94.4%) of 18 E-cadherin-reduced tissues. Our results suggest thatreduction of E-cadherin expression is associated with CpG methylation of the E-cadherin gene promoter. We recently established two cell lines with high and low metastatic potential, UM I and UM2, from SCC primary tongue tissue of a patient. E-cadherin expression of high-metastatic UM I was clearly lower than that of low-metastatic UM2, and MSP results showed CpG methylation in the UM I but not the UM2 cell line. To investigate whether demethylation of CpG methylation of the E-cadherin gene could restore expression and function of E-cadherin, we treated UM I with the demethylating agent S-azacytidine (5-aza) and found that E-cadherin expression was indeed restored bydemethylation. Moreover, in the demethylated UM 1, invasion of the collagen gel was clearly suppressed compared with the untreated UM 1. These results suggested that inactivation of E-cadherin expression resulted from CpG methylation of the gene promoter; a correlation between CpG methylation of the E-cadherin gene promoter and invasive potential was also suggested. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 02:48:46