Overexpression of HDAC1 induces cellular senescence by Sp1/PP2A/pRb pathway

Jian Ying Chuang, Jan Jong Hung

研究成果: 雜誌貢獻文章

19 引文 (Scopus)

摘要

Senescence is associated with decreased activities of DNA replication, protein synthesis, and cellular division, which can result in deterioration of cellular functions. Herein, we report that the growth and division of tumor cells were significantly repressed by overexpression of histone deacetylase (HDAC) 1 with the Tet-off induced system or transient transfection. In addition, HDAC1 overexpression led to senescence through both an accumulation of hypophosphorylated active retinoblastoma protein (pRb) and an increase in the protein level of protein phosphatase 2A catalytic subunit (PP2Ac). HDAC1 overexpression also increased the level of Sp1 deacetylation and elevated the interaction between Sp1 and p300, and subsequently that Sp1/p300 complex bound to the promoter of PP2Ac, thus leading to induction of PP2Ac expression. Similar results were obtained in the HDAC1-Tet-off stable clone. Taken together, these results indicate that HDAC1 overexpression restrained cell proliferation and induced premature senescence in cervical cancer cells through a novel Sp1/PP2A/pRb pathway.
原文英語
頁(從 - 到)587-592
頁數6
期刊Biochemical and Biophysical Research Communications
407
發行號3
DOIs
出版狀態已發佈 - 四月 15 2011
對外發佈Yes

指紋

Protein Phosphatase 2
Cell Aging
Catalytic Domain
Histone Deacetylase 1
Cells
Retinoblastoma Protein
Cell proliferation
DNA Replication
Uterine Cervical Neoplasms
Cell Division
Transfection
Deterioration
Tumors
Proteins
Clone Cells
Cell Proliferation
DNA
Growth
Neoplasms

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology

引用此文

Overexpression of HDAC1 induces cellular senescence by Sp1/PP2A/pRb pathway. / Chuang, Jian Ying; Hung, Jan Jong.

於: Biochemical and Biophysical Research Communications, 卷 407, 編號 3, 15.04.2011, p. 587-592.

研究成果: 雜誌貢獻文章

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abstract = "Senescence is associated with decreased activities of DNA replication, protein synthesis, and cellular division, which can result in deterioration of cellular functions. Herein, we report that the growth and division of tumor cells were significantly repressed by overexpression of histone deacetylase (HDAC) 1 with the Tet-off induced system or transient transfection. In addition, HDAC1 overexpression led to senescence through both an accumulation of hypophosphorylated active retinoblastoma protein (pRb) and an increase in the protein level of protein phosphatase 2A catalytic subunit (PP2Ac). HDAC1 overexpression also increased the level of Sp1 deacetylation and elevated the interaction between Sp1 and p300, and subsequently that Sp1/p300 complex bound to the promoter of PP2Ac, thus leading to induction of PP2Ac expression. Similar results were obtained in the HDAC1-Tet-off stable clone. Taken together, these results indicate that HDAC1 overexpression restrained cell proliferation and induced premature senescence in cervical cancer cells through a novel Sp1/PP2A/pRb pathway.",
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