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Tumor Biology

, Volume 36, Issue 3, pp 1471–1476 | Cite as

Activating transcription factor 3 interferes with p21 activation in histone deacetylase inhibitor-induced growth inhibition of epidermoid carcinoma cells

  • Zhen-Feng Hao
  • You-Ming Su
  • Cong-min Wang
  • Rong-Ya Yang
Research Article
  • 228 Downloads

Abstract

Inhibition of histone deacetylase (HDAC) activity by HDAC inhibitors (HDACis) results in cancer cell growth inhibition, and HDACis have been revealed as potential anti-skin cancer agents. p21 is a cyclin-dependent kinase inhibitor and an essential regulator of growth inhibition. Recently, we reported that activating transcription factor 3 (ATF3) could significantly promote skin cancer cell growth. This study explored the relationship between ATF3 and HDACi-induced growth inhibition of epidermoid carcinoma cells. We found that trichostatin A (TSA) treatment inhibited cell growth in A431 epidermoid carcinoma cells in a dose-dependent manner. Simultaneously, p21 and ATF3 expression levels were upregulated and downregulated upon TSA stimulation, respectively. ATF3 overexpression promoted cell growth and downregulated p21 expression. In contrast, ATF3 depletion resulted in cell growth reduction and p21 transcriptional upregulation. More importantly, ATF3 overexpression partially antagonized TSA-induced growth inhibition and p21 activation. Collectively, these data demonstrate that ATF3 acts as an essential negative regulator of TSA-induced cell growth inhibition through interfering with TSA-induced p21 activation.

Keywords

ATF3 p21 HDAC Growth inhibition Epidermoid carcinoma cell 

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Copyright information

© International Society of Oncology and BioMarkers (ISOBM) 2014

Authors and Affiliations

  • Zhen-Feng Hao
    • 1
    • 2
  • You-Ming Su
    • 1
  • Cong-min Wang
    • 1
  • Rong-Ya Yang
    • 1
  1. 1.Institute of Skin Damage and RepairGeneral Hospital of Beijing Region of PLABeijingChina
  2. 2.Graduate Management BrigadeThird Military Medical UniversityChongqingChina

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