Down-regulation of the cyclin A promoter in differentiating human embryonal carcinoma cells is mediated by depletion of ATF-1 and ATF-2 in the complex at the ATF/CRE site

Exp Cell Res. 1995 Feb;216(2):422-30. doi: 10.1006/excr.1995.1053.

Abstract

The human embryonal carcinoma cell line NEC14 can be induced to differentiate by the addition of N,N'-hexamethylene-bis-acetamide (HMBA). After treatment with HMBA, the level of cyclin A transcript decreased steeply, reaching less than one-tenth of the original level by 48 h. The promoter elements concerned with this down-regulation were studied by using reporter genes and by analyzing DNA-protein complexes. The deletion of the sequence between -608 and -259 containing three GC boxes decreased the promoter activity to about a half, and further deletion up to -194, eliminating the ATF/CRE site, resulted in a decrease to about a tenth of the original level in undifferentiated NEC14 cells. These sequences were involved in down-regulation of the promoter activity in differentiation-induced NEC14 cells. DNA-protein complexes formed at the ATF/CRE site with extracts prepared from undifferentiated and differentiation-induced cells gave the same footprint, but showed different electrophoretic mobilities. The supershift assay with specific antibodies against ATF-1 and ATF-2 indicated that both factors were depleted in the complex after induction of NEC14 cell differentiation. Both the ATF/CRE site and GC boxes seemed to be also involved in up-regulation of the cyclin A promoter in growth-stimulated human fibroblasts at the G1/S boundary.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetamides / pharmacology
  • Activating Transcription Factor 2
  • Activating Transcription Factors
  • Base Sequence
  • Blood Proteins / metabolism*
  • Carcinoma, Embryonal
  • Cell Cycle
  • Cell Differentiation* / drug effects
  • Cyclic AMP Response Element-Binding Protein / metabolism*
  • Cyclins / genetics*
  • DNA, Neoplasm / metabolism
  • Down-Regulation / physiology*
  • Fibroblasts / cytology
  • Fibroblasts / metabolism
  • Genes, Reporter / genetics
  • Humans
  • Leucine Zippers / genetics
  • Molecular Sequence Data
  • Nuclear Proteins / metabolism
  • Promoter Regions, Genetic / genetics*
  • RNA, Messenger / biosynthesis
  • Recombinant Fusion Proteins / biosynthesis
  • Sequence Analysis, DNA
  • Sequence Deletion / physiology
  • Transcription Factors / metabolism*
  • Tumor Cells, Cultured

Substances

  • ATF2 protein, human
  • Acetamides
  • Activating Transcription Factor 2
  • Activating Transcription Factors
  • Blood Proteins
  • Cyclic AMP Response Element-Binding Protein
  • Cyclins
  • DNA, Neoplasm
  • Nuclear Proteins
  • RNA, Messenger
  • Recombinant Fusion Proteins
  • Transcription Factors
  • hexamethylene bisacetamide