Tumor cells exhibit deregulation of the cell cycle histone gene promoter factor HiNF-D

Joost Holthuis, Thomas A. Owen, André J. Van Wijnen, Kenneth L. Wright, Anna Ramsey-Ewing, Mary Beth Kennedy, Ruth Carter, Stephen C. Cosenza, Kenneth J. Soprano, Jane B. Lian, Janet L. Stein, Gary S. Stein

Research output: Contribution to journalArticlepeer-review

85 Scopus citations


Cell cycle - regulated gene expression is essential for normal cell growth and development and loss of stringent growth control is associated with the acquisition of the transformed phenotype. The selective synthesis of histone proteins during the S phase of the cell cycle is required to render cells competent for the ordered packaging of replicating DNA into chromatin. Regulation of H4 histone gene transcription requires the proliferation-specific promoter binding factor HiNF-D. In normal diploid cells, HiNF-D binding activity is regulated during the cell cycle; nuclear protein extracts prepared from normal cells in S phase contain distinct and measurable HiNF-D binding activity, while this activity is barely detectable in Gl phase cells. In contrast, in tumor-derived or transformed cell lines, HiNF-D binding activity is constitutively elevated throughout the cell cycle and declines only with the onset of differentiation. The change from cell cycle - mediated to constitutive interaction of HiNF-D with the promoter of a cell growth - controlled gene is consistent with, and may be functionally related to, the loss of stringent cell growth regulation associated with neoplastic transformation.

Original languageEnglish (US)
Pages (from-to)1454-1457
Number of pages4
Issue number4949
StatePublished - 1990

ASJC Scopus subject areas

  • General


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