Histone deacetylase inhibitors reduce WB-F344 oval cell viability and migration capability by suppressing AKT/mTOR signaling in vitro

Peng Zhang, Xiaofeng Zhu, Ying Wu, Ronglin Hu, Dongming Li, Jun Du, Xingyuan Jiao, Xiaoshun He

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Histone deacetylase (HDAC) can blockDNA replication and transcription and altered HDAC expression was associated with tumorigenesis. This study investigated the effects of HDAC inhibitors on hepatic oval cells and aimed to delineate the underlying molecular events. Hepatic oval cells were treated with two different HDAC inhibitors, suberoylanilidehydroxamic acid (SAHA) and trichostatin-A (TSA). Cells were subjected to cell morphology, cell viability, cell cycle, and wound healing assays. The expression of proteins related to both apoptosis and the cell cycle, and proteins of the AKT/mammalian target of rapamycin (mTOR) signaling pathway were analyzed by Western blot. The data showed that HDAC inhibitors reduced oval cell viability and migration capability, and arrested oval cells at the G0/G1 and S phases of the cell cycle, in a dose- and time-dependent manner. HDAC inhibitors altered cell morphology and reduced oval cell viability, and downregulated the expression of PCNA, cyclinD1, c-Myc and Bmi1 proteins, while also suppressing AKT/mTOR and its downstream target activity. In conclusion, this study demonstrates that HDAC inhibitors affect oval cells by suppressing AKT/mTOR signaling.

Original languageEnglish (US)
Pages (from-to)1-9
Number of pages9
JournalArchives of Biochemistry and Biophysics
Volume590
DOIs
StatePublished - Jan 15 2016

Keywords

  • AKT/mTOR signaling pathway
  • Apoptosis
  • Cell proliferation
  • Histone deacetylase inhibitor
  • Oval cells
  • Rapamycin

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology

Fingerprint Dive into the research topics of 'Histone deacetylase inhibitors reduce WB-F344 oval cell viability and migration capability by suppressing AKT/mTOR signaling in vitro'. Together they form a unique fingerprint.

Cite this