PLU1 histone demethylase decreases the expression of KAT5 and enhances the invasive activity of the cells
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- Masakazu Yoshida
- Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa 920-1192, Ishikawa, Japan
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- Akihiko Ishimura
- Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa 920-1192, Ishikawa, Japan
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- Minoru Terashima
- Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa 920-1192, Ishikawa, Japan
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- Zanabazar Enkhbaatar
- Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa 920-1192, Ishikawa, Japan
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- Naohito Nozaki
- Bio-Frontier Research Center, Tokyo Institute of Technology, Yokohama 226-8503, Kanagawa, Japan
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- Kenji Satou
- Division of Electrical Engineering and Computer Science, Graduate School of Natural Science and Technology, Kanazawa University, Kanazawa 920-1192, Ishikawa, Japan
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- Takeshi Suzuki
- Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kanazawa 920-1192, Ishikawa, Japan
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説明
<jats:p>PLU1 is a candidate oncogene that encodes H3K4 (Lys4 of histone H3) demethylase. In the present study, we found that ectopic expression of PLU1 enhanced the invasive potential of the weakly invasive cells dependent on its demethylase activity. PLU1 was shown to repress the expression of the KAT5 gene through its H3K4 demethylation on the promoter. The regulation of KAT5 by PLU1 was suggested to be responsible for PLU1-induced cell invasion. First, knockdown of KAT5 similarly increased the invasive potential of the cells. Secondly, knockdown of PLU1 in the highly invasive cancer cells increased KAT5 expression and reduced the invasive activity. Thirdly, simultaneous knockdown of KAT5 partially relieved the suppression of cell invasion imposed by PLU1 knockdown. Finally, we found that CD82, which was transcriptionally regulated by KAT5, might be a candidate effector of cell invasion promoted by PLU1. The present study demonstrated a functional contribution of PLU1 overexpression with concomitant epigenetic dysregulation in cancer progression.</jats:p>
収録刊行物
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- Biochemical Journal
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Biochemical Journal 437 (3), 555-564, 2011-07-13
Portland Press Ltd.
