Gene Expression Analysis in Human Gastric Cancer Cell Line Treated with Trichostatin A and S-Adenosyl-L-homocysteine Using cDNA Microarray

  • Lee Heun-Sik
    Laboratory of Human Genetics, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Park Mie-Hee
    Laboratory of Human Genetics, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Yang Suk-Jin
    Laboratory of Human Genetics, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Jung Hai-Young
    Laboratory of Human Genetics, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Byun Sang-Soon
    Laboratory of Human Genetics, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Lee Dong-Seok
    Laboratory of Human Genetics, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Yoo Hyang-Sook
    Laboratory of Human Genetics, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Yeom Young Il
    Laboratory of Human Genetics, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Seo Sang-Beom
    Cell & Developmental Biology and Dental Research Institute, College of Dentistry, Seoul National University

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Description

Trichostatin A (TSA) and S-adenosyl-L-homocysteine (AdoHcy) have been reported to affect histone modifications. To investigate the effects of two drugs that can reportedly affect chromatin remodeling, we analyzed the gene expression profiles of TSA and AdoHcy in a gastric cancer cell line using 14 K cDNA microarray. The significant analysis of microarray (SAM) identified 98 and 43 differentially expressed genes in TSA and AdoHcy treated sets, respectively, and selected genes were functionally classified. In the gastric cancer cell line, genes related to cell communication, cell growth/maintenance, and morphogenesis were highly expressed with TSA, and genes with cell growth/maintenance, metabolism, oxidoreductase activity were upregulated with AdoHcy. Genes downregulated with TSA included those controlling the cell cycle, cell growth/proliferation, DNA binding, and metabolism, whereas genes involved in calcium signaling, cell growth/proliferation, and metabolism were downregulated with AdoHcy. Furthermore, we identified the genes commonly expressed in both drug treatments. Compared to TSA, AdoHcy did not induce apoptosis in the SNU-16 gastric cancer cell line, and RT-PCR was performed for selective genes to confirm the microarray data. This gene expression profile analysis with TSA and AdoHcy should contribute to a greater understanding of the molecular mechanism of chromatin remodeling and cancer, and provide candidate genes for further studies involving the roles of histone modifications in gastric cancer.

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