Literature DB >> 19850045

The histone demethylase RBP2 Is overexpressed in gastric cancer and its inhibition triggers senescence of cancer cells.

Jiping Zeng1, Zheng Ge, Lixiang Wang, Qiao Li, Na Wang, Magnus Björkholm, Jihui Jia, Dawei Xu.   

Abstract

BACKGROUND & AIMS: The aberrant expression of histone-modifying enzymes such as histone deacetylases contributes to oncogenesis. It is unclear whether RBP2, a newly identified histone demethylase, is involved in cancer development/progression. We determined RBP2 expression in gastric cancer and its biologic function in cancer cells.
METHODS: Cancerous and matched normal gastric specimens from 42 patients with gastric cancer were analyzed for RBP2 expression using quantitative real-time polymerase chain reaction and immunohistochemistry. Gene expression was assessed using quantitative real-time polymerase chain reaction and immunoblotting and depleted with small interference RNA. Clonogenesis and cellular senescence were examined by foci formation and beta-Galactosidase staining. Promoter activity was determined by luciferase reporter assay. Chromatin immunoprecipitation was used to detect RBP2 and methylated histone H3-K4 on promoters.
RESULTS: RBP2 messenger RNA and protein expression were increased in 71.5% (30/42) and 100% (20/20) of gastric cancer specimens, respectively. Significantly diminished foci numbers coupled with massive senescence/growth arrest and elevated expression of cyclin-dependent kinase inhibitors (CDKIs) p21(CIP1), p27(kip1), and/or p16(ink4a) occurred in RBP2-depleted gastric and cervical cancer cells. RBP2 depletion-mediated senescence and clonogenic defect were attenuated by inhibiting p21(CIP1) or p27(kip1) expression. The promoter activity of all 3 CDKIs genes was enhanced by RBP2 inhibition. RBP2 occupied these promoters in control cells, and the loss of RBP2 occupancy was accompanied by enhanced H3-K4 trimethylation following RBP2 depletion.
CONCLUSIONS: RBP2 is overexpressed in gastric cancer, and its inhibition triggers senescence of malignant cells at least partially by derepressing its target genes CDKIs. Histone demethylase inhibition by targeting RBP2 may be an anticancer strategy. Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.

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Year:  2009        PMID: 19850045     DOI: 10.1053/j.gastro.2009.10.004

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  71 in total

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Review 9.  Histone lysine-specific methyltransferases and demethylases in carcinogenesis: new targets for cancer therapy and prevention.

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Review 10.  DNA and histone methylation in gastric carcinogenesis.

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Journal:  World J Gastroenterol       Date:  2013-02-28       Impact factor: 5.742

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