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Title 

Downregulation of gelsolin and retinoic acid receptor β expression in gastric cancer tissues through histone deacetylase 1

Authors 

J H KimYang Kyu ChoiH J KwonH K YangJae Hoon ChoiD Y Kim

Publisher 

Wiley-Blackwell

Issue Date 

2004

Citation 

Journal of Gastroenterology and Hepatology, vol. 19, no. 2, pp. 218-224

Keywords 

gastric cancergelsolinhistone deacetylase 1retinoic acid receptor βhistone deacetylaseretinoic acid receptor betacancer tissuehuman tissueprotein expressionreceptor down regulation

Abstract 

Background and Aim: Overexpression of histone deacetylase (HDAC)1, which controls the expression of genes related to cell cycle and apoptosis, has recently been reported in gastric cancer (GC) tissues. In the present study, the pattern of gelsolin and retinoic acid receptor (RAR)β expression in GC tissues showing HDAC1 overexpression was investigated. Methods: Expression profiles of HDAC1, gelsolin, and RARβ were evaluated and compared using reverse transcription-polymerase chain reaction, immunoblotting, and immunohistochemical analyses with 22 paired primary human GC tissues and corresponding normal tissues. Results: Compared with normal gastric tissue, increased expression of HDAC1 mRNA and protein was detected in 17 (77.3%) of 22 GC tissues, while decreased expressions of gelsolin mRNA and protein were shown in 15 (68.1%) samples. Concomitantly, expressions of RARβ mRNA and protein were decreased in 16 (72.7%) and 17 (77.3%), respectively. Among 17 GC tissues with increased HDAC1 expression, the expressions of gelsolin and RARβ were simultaneously decreased in 14 (82.4%) and 15 (88.2%) GC tissues, which indicates a strong inverse correlation between HDAC1 and gelsolin/ RARβ expressions. Correlation between HDAC1 and gelsolin/RARβ was also confirmed by immunohistochemistry. Conclusions: Taken together, the results of the present study reveal that silencing of gelsolin and RARβ occurs in GC tissues probably through HDAC1 overexpression and might play some role in gastric carcinogenesis.

ISSN 

0815-9319

Link 

http://dx.doi.org/10.1111/j.1440-1746.2004.03336.x

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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