Linked Life Data

1334691

Source:http://linkedlifedata.com/resource/pubmed/id/1334691

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1993-1-25
pubmed:abstractText
The role of transforming growth factor beta 1 (TGF-beta 1) in enterocytic differentiation was examined by treating two undifferentiated HT29 colon carcinoma sublines, U4 and U9, with hexamethylene bisacetamide to up-regulate their level of TGF-beta 1 mRNA expression. Although both lines after treatment secreted approximately equal levels of biologically active TGF-beta 1, only U4H cells were found to undergo enterocytic differentiation when cultured postconfluence on collagen I-coated transwells, forming polarized monolayer cells with an apical brush border, whereas U9H cells remained multilayered and undifferentiated. Enterocytic U4H cells exhibited four times as much cell surface expression of the collagen I-binding protein alpha 2-integrin, twice as much of the accessory collagen-binding protein carcinoembryonic antigen, and almost twice as much binding to collagen I films as undifferentiated U9H cells. TGF-beta 1 treatment doubled U4 cell collagen I binding, increased expression of alpha 2-integrin 4-fold, but increased carcinoembryonic antigen expression only marginally. U4H cells displayed cell cycle regulation by arresting reversibly at a restriction point in G1 when placed in the postconfluent culture conditions which initiated enterocytic differentiation. In contrast, undifferentiated U9H cells exhibited no restriction point but arrested throughout G1. TGF-beta 1 blocked synchronized U4H cells in G1, whereas it stimulated the growth of U9H cells. Thus, TGF-beta 1 has two roles in enterocytic differentiation: to increase levels of collagen I adhesion proteins and to block enterocytic cells in G1 so that they can differentiate.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1044-9523
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
753-62
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1334691-Acetamides, pubmed-meshheading:1334691-Carcinoembryonic Antigen, pubmed-meshheading:1334691-Carcinoma, pubmed-meshheading:1334691-Cell Adhesion, pubmed-meshheading:1334691-Cell Differentiation, pubmed-meshheading:1334691-Colon, pubmed-meshheading:1334691-Colonic Neoplasms, pubmed-meshheading:1334691-Gene Expression Regulation, Neoplastic, pubmed-meshheading:1334691-Humans, pubmed-meshheading:1334691-Integrins, pubmed-meshheading:1334691-Interphase, pubmed-meshheading:1334691-Neoplasm Proteins, pubmed-meshheading:1334691-RNA, Messenger, pubmed-meshheading:1334691-RNA, Neoplasm, pubmed-meshheading:1334691-Receptors, Cell Surface, pubmed-meshheading:1334691-Receptors, Collagen, pubmed-meshheading:1334691-Transforming Growth Factor beta, pubmed-meshheading:1334691-Tumor Cells, Cultured
pubmed:year
1992
pubmed:articleTitle
Two roles for transforming growth factor beta 1 in colon enterocytic cell differentiation.
pubmed:affiliation
Laboratory of Gastrointestinal Tumor Biology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't