Frequent hypermethylation of CpG islands and loss of expression of the 14-3-3 σ gene in human hepatocellular carcinoma View Full Text


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Article Info

DATE

2000-11-02

AUTHORS

Norikazu Iwata, Hiroyuki Yamamoto, Shigeru Sasaki, Fumio Itoh, Hiromu Suzuki, Takefumi Kikuchi, Hiroyuki Kaneto, Shouhei Iku, Itaru Ozeki, Yoshiyasu Karino, Toshihiro Satoh, Joji Toyota, Masaaki Satoh, Takao Endo, Kohzoh Imai

ABSTRACT

The 14-3-3 σ gene has been implicated in G2/M cell cycle arrest by p53. Frequent inactivation of the 14-3-3 σ gene by hypermethylation of CpG islands has recently been reported in human breast carcinoma. The aim of this study was to examine the methylation status of CpG islands of the 14-3-3 σ gene in hepatocellular carcinoma (HCC). The methylation status of the 14-3-3 σ gene was evaluated in four normal liver tissues and 19 paired specimens of carcinoma and adjacent non-tumorous liver tissues using bisulfite-single strand conformation polymorphism (bisulfite-SSCP), a combination of sodium bisulfite modification and fluorescence-based polymerase chain reaction (PCR)-SSCP. The 14-3-3 σ protein expression was examined by immunohistochemical staining. Hypermethylation of CpG islands of the 14-3-3 σ gene was detected in 89% (17/19) of the HCC tissues but not in any of the four normal liver tissues. All of the 14 methylation-positive HCC samples analysed by immunohistochemistry showed loss of 14-3-3 σ expression, while both of the methylation-negative HCC samples retained the expression, and a significant correlation was found between methylation and loss of expression. Lower levels of methylation were detected in adjacent non-tumorous liver tissues (6/16 in cirrhotic tissues and 1/3 in chronic hepatitis tissues), but the 14-3-3 σ expression was retained in all of these tissues. In a methylation-positive HCC cell line, HLE, 5-aza-2′-deoxycytidine (5-aza-dC)-induced demethylation of CpG islands led to reactivation of gene expression, indicating that hypermethylation plays a causal role in inactivation of the 14-3-3 σ gene in HCC. Hypermethylation and the resulting loss of expression of the 14-3-3 σ gene corresponds to one of the most common abnormalities reported to date in HCC, suggesting their crucial role in the development and/or progression of HCC. More... »

PAGES

5298-5302

References to SciGraph publications

  • 1999-10. 14-3-3σ is required to prevent mitotic catastrophe after DNA damage in NATURE
  • 1997-06-19. Comprehensive allelotyping of human hepatocellular carcinoma in ONCOGENE
  • 1999-10. Fools rush in in NATURE
  • <error retrieving object. in <ERROR RETRIEVING OBJECT
  • 1999-11. Asteroidal defence in NATURE
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/sj.onc.1203898

    DOI

    http://dx.doi.org/10.1038/sj.onc.1203898

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1029696632

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/11077447


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    28 schema:description The 14-3-3 σ gene has been implicated in G2/M cell cycle arrest by p53. Frequent inactivation of the 14-3-3 σ gene by hypermethylation of CpG islands has recently been reported in human breast carcinoma. The aim of this study was to examine the methylation status of CpG islands of the 14-3-3 σ gene in hepatocellular carcinoma (HCC). The methylation status of the 14-3-3 σ gene was evaluated in four normal liver tissues and 19 paired specimens of carcinoma and adjacent non-tumorous liver tissues using bisulfite-single strand conformation polymorphism (bisulfite-SSCP), a combination of sodium bisulfite modification and fluorescence-based polymerase chain reaction (PCR)-SSCP. The 14-3-3 σ protein expression was examined by immunohistochemical staining. Hypermethylation of CpG islands of the 14-3-3 σ gene was detected in 89% (17/19) of the HCC tissues but not in any of the four normal liver tissues. All of the 14 methylation-positive HCC samples analysed by immunohistochemistry showed loss of 14-3-3 σ expression, while both of the methylation-negative HCC samples retained the expression, and a significant correlation was found between methylation and loss of expression. Lower levels of methylation were detected in adjacent non-tumorous liver tissues (6/16 in cirrhotic tissues and 1/3 in chronic hepatitis tissues), but the 14-3-3 σ expression was retained in all of these tissues. In a methylation-positive HCC cell line, HLE, 5-aza-2′-deoxycytidine (5-aza-dC)-induced demethylation of CpG islands led to reactivation of gene expression, indicating that hypermethylation plays a causal role in inactivation of the 14-3-3 σ gene in HCC. Hypermethylation and the resulting loss of expression of the 14-3-3 σ gene corresponds to one of the most common abnormalities reported to date in HCC, suggesting their crucial role in the development and/or progression of HCC.
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