PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation

E. Suzuki, I. Imoto, A. Pimkhaokham, T. Nakagawa, N. Kamata, K. I. Kozaki, T. Amagasa, J. Inazawa

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Array-based comparative genomic hybridization (array-CGH) has good potential for the high-throughput identification of genetic aberrations in cell genomes. In the course of a program to screen a panel of oral squamous-cell carcinoma (OSCC), cell lines for genomic copy-number aberrations by array-CGH using our in-house arrays, we identified a 3-Mb homozygous deletion at 10p12 in 1 of 18 cell lines (5.6%). Among seven genes located within this region, expression of PRTFDC1 mRNA was not detected in 50% (9/18) or decreased in 5.6% (1/18) of OSCC cell lines, but detected in normal oral epithelia and restored in gene-silenced OSCC cells without its homozygous loss after treatment with 5-aza-2′-deoxycytidine. Among 17 cell lines without a homozygous deletion, the hypermethylation of the PRTFDC1 CpG island, which showed promoter activity, was observed in all nine cell lines with no or reduced PRTFDC1 expression (52.9%). Methylation of this CpG island was also observed in primary OSCC tissues (8/47, 17.0%). In addition, restoration of PRTFDC1 in OSCC cells lacking its expression inhibited cell growth in colony-formation assays, whereas knockdown of PRTFDC1 expression in OSCC cells expressing the gene promoted cell growth. These results suggest that epigenetic silencing of PRTFDC1 by hypermethylation of the CpG island leads to a loss of PRTFDC1 function, which might be involved in squamous cell oral carcinogenesis.

Original languageEnglish
Pages (from-to)7921-7932
Number of pages12
JournalOncogene
Volume26
Issue number57
DOIs
Publication statusPublished - Dec 13 2007
Externally publishedYes

Fingerprint

Tumor Suppressor Genes
Squamous Cell Carcinoma
CpG Islands
Cell Line
Comparative Genomic Hybridization
decitabine
Genes
Growth
Epigenomics
Methylation
Carcinogenesis
Epithelium
Epithelial Cells
Genome
Messenger RNA

Keywords

  • Array-CGH
  • Homozygous deletion
  • Methylation
  • Oral squamous-cell carcinoma
  • PRTFDC1

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

Cite this

Suzuki, E., Imoto, I., Pimkhaokham, A., Nakagawa, T., Kamata, N., Kozaki, K. I., ... Inazawa, J. (2007). PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation. Oncogene, 26(57), 7921-7932. https://doi.org/10.1038/sj.onc.1210589

PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation. / Suzuki, E.; Imoto, I.; Pimkhaokham, A.; Nakagawa, T.; Kamata, N.; Kozaki, K. I.; Amagasa, T.; Inazawa, J.

In: Oncogene, Vol. 26, No. 57, 13.12.2007, p. 7921-7932.

Research output: Contribution to journalArticle

Suzuki, E, Imoto, I, Pimkhaokham, A, Nakagawa, T, Kamata, N, Kozaki, KI, Amagasa, T & Inazawa, J 2007, 'PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation', Oncogene, vol. 26, no. 57, pp. 7921-7932. https://doi.org/10.1038/sj.onc.1210589
Suzuki, E. ; Imoto, I. ; Pimkhaokham, A. ; Nakagawa, T. ; Kamata, N. ; Kozaki, K. I. ; Amagasa, T. ; Inazawa, J. / PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation. In: Oncogene. 2007 ; Vol. 26, No. 57. pp. 7921-7932.
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AU - Nakagawa, T.

AU - Kamata, N.

AU - Kozaki, K. I.

AU - Amagasa, T.

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