The mechanisms by which a human apolipoprotein B gene enhancer and reducer interact with the promoter are different in cultured cells of hepatic and intestinal origin

J Biol Chem. 1991 Dec 15;266(35):24161-8.

Abstract

In the preceding paper (Paulweber, B., Onasch, M. A., Nagy, B. P., and Levy-Wilson, B. (1991) J. Biol. Chem. 266, 24149-24160) we demonstrated that the segment of the apolipoprotein B promoter extending from -260 to -85 is functionally different in hepatic (HepG2) and intestinal (CaCo-2) cells. These functional differences could be explained at least in part by differences in binding of three nuclear proteins to the region from -111 to -88. In this article we present further evidence suggesting that the mechanisms involved in transcriptional control of the apolipoprotein B gene in HepG2 and CaCo-2 cells are different, by demonstrating that an enhancer and a reducer can alter the activity of various apolipoprotein B promoter segments in widely differing ways in these two cell lines. Furthermore, we have localized a 329-base pair segment that is found within a negative regulatory region in the 5' distal portion of the gene. It displays a strong reducer effect upon promoter sequences that exhibit maximal transcriptional activity in CaCo-2 cells, but not in HepG2 cells.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Apolipoproteins B / genetics*
  • Base Sequence
  • Carcinoma, Hepatocellular
  • Cell Line
  • Chloramphenicol O-Acetyltransferase / genetics
  • Chloramphenicol O-Acetyltransferase / metabolism
  • Chromosome Deletion
  • Colonic Neoplasms
  • DNA, Neoplasm / genetics
  • DNA, Neoplasm / isolation & purification
  • Deoxyribonuclease I
  • Enhancer Elements, Genetic*
  • Genes
  • Humans
  • Liver Neoplasms
  • Models, Genetic
  • Molecular Sequence Data
  • Plasmids
  • Promoter Regions, Genetic
  • Recombinant Fusion Proteins / metabolism
  • Regulatory Sequences, Nucleic Acid
  • Restriction Mapping
  • Transfection

Substances

  • Apolipoproteins B
  • DNA, Neoplasm
  • Recombinant Fusion Proteins
  • Chloramphenicol O-Acetyltransferase
  • Deoxyribonuclease I