Trichostatin A inhibits β-casein expression in mammary epithelial cells

Philippe Pujuguet, Derek Radisky, Dinah Levy, Charlemagne Lacza, Mina J. Bissell

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


Many aspects of cellular behavior are defined by the content of information provided by association of the extracellular matrix (ECM) and with cell membrane receptors. When cultured in the presence of laminin-containing ECM and prolactin (Prl), normal mammary epithelial cells express the milk protein β-casein. We have previously found that the minimal ECM- and Prl-responsive enhancer element BCE-1 was only active when stably integrated into chromatin, and that trichostatin A (TSA), a reagent that leads to alterations in chromatin structure, was able to activate the integrated enhancer element. We now show that endogenous β-casein gene, which is controlled by a genetic assembly that is highly similar to that of BCE-1 and which is also activated by incubation in ECM and Prl, is instead inhibited by TSA. We provide evidence that the differing response of β-casein and BCE-1 to TSA is neither due to an unusual effect of TSA on mammary epithelial cells, nor to secondary consequences from the expression of a separate gene, nor to a particular property of the BCE-1 construct. As a component of this investigation, we also showed that ECM mediated rapid histone deacetylation in mammary epithelial cells. These results are discussed in combination with previous work showing that TSA mediates the differentiation of many types of cancer cells but inhibits differentiation of some nonmalignant cell types.

Original languageEnglish (US)
Pages (from-to)660-670
Number of pages11
JournalJournal of cellular biochemistry
Issue number4
StatePublished - 2001


  • Basement membrane
  • Chromatin structure
  • Extracellular matrix
  • Histone H4
  • Tissue specificity

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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