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  • Title: Expression of plasminogen activator inhibitor type 1 (PAI-1) by HT-29di human large bowel carcinoma cells is modulated as a function of epithelial differentiation.
    Author: Higgins PJ, Lipkin M.
    Journal: Cancer Lett; 1994 Jan 30; 76(2-3):167-75. PubMed ID: 8149346.
    Abstract:
    Highly differentiated epithelial populations (36% mucin-producing cells; sixfold increase in alkaline phosphatase activity; development of flat, substrate-adherent, entero-cytic foci) were induced upon in vitro exposure of HT-29di human colon carcinoma cells to sodium butyrate (NaB). 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] (10(-7) M) and the ionophore A23187 (0.5 microM) significantly augmented (two to threefold) NaB-induced HT-29di differentiation, whereas 1,25-(OH)2D3 or A23187 alone were not effective. Induction reflected specific changes in protein abundance, involving, most notably, a differentiation-associated increase in the expression and substrate-deposition of a 47-kDa protein with pI/mw two-dimensional map coordinates and immunochemical properties identical to that of plasminogen activator inhibitor type 1 (PAI-1), a major regulator of the pericellular proteolytic cascade. Culture of HT-29di cells in medium of either high (2.5 mM) or low (0.25 mM) Ca2+ concentration did not affect the incidence of 'spontaneous' differentiation, although NaB-induced goblet cell and enterocytic maturation was Ca(2+)-dependent. The inability of 1,25-(OH)2D3, A23187 or modulated Ca2+ levels alone (i.e., in the absence of NaB) to effect differentiation of HT-29di cells and the Ca(2+)-dependence of the NaB response indicate that NaB and Ca2+ act co-operatively to induce colonic epithelial maturation in vitro.
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