Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 83, Issue 4, Pages 660-670Publisher
WILEY
DOI: 10.1002/jcb.1260
Keywords
tissue specificity; histone H4; basement membrane; extracellular matrix; chromatin structure
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Funding
- NCI NIH HHS [R01 CA057621, R01 CA057621-11, CA-57621-02] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA057621] Funding Source: NIH RePORTER
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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 epithelia] cells express the milk protein beta -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 beta -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 beta -casein and BCE-1 to TSA is neither due to an unusual effect of TSA on mammary epithelia[ 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. (C) 2001 Wiley-Liss, Inc.
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