Document Detail


Pit cells (Hepatic natural killer cells) of the rat induce apoptosis in colon carcinoma cells by the perforin/granzyme pathway.
MedLine Citation:
PMID:  9862849     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The high mortality of colon cancer is to a large extent caused by the frequent occurrence of liver metastasis. This is remarkable, because the liver harbors two distinct cell populations that can eliminate invading cancer cells, namely hepatic natural killer (NK) cells and Kupffer cells. These hepatic NK cells, known as pit cells, are the most cytotoxic cells of the naturally occurring NK cells. However, the mechanism by which pit cells eliminate tumor cells is largely unknown. Because we recently found an indication that apoptosis is involved, we tried to assess the role of this mode of cell death using an in vitro system with isolated pure pit cells (>90%) and CC531s cells, a rat colon carcinoma (CC) cell line. Pit cells induced apoptosis in CC531s cells as shown by quantitative DNA fragmentation, agarose gel electrophoresis, and different modes of microscopy. When extracellular Ca2+ was chelated by ethylene glycol-bis(beta-aminoethyl ether)-N,N,-tetraacetic acid (EGTA) during coincubation or when the pit cells were preincubated with the granzyme inhibitor 3,4-dichloroisocoumarin (DCI), the induction of apoptosis was abolished. These results show that pit cells use the Ca2+-dependent perforin/granzyme pathway to induce apoptosis in the CC531s cells, and not the alternative Ca2+-independent Fas pathway. To further exclude the possibility of the involvement of the Fas pathway, we treated CC531s cells with recombinant Fas ligand. This treatment did not result in the induction of apoptosis, indicating that CC531s cells are resistant to Fas-mediated apoptosis. We conclude therefore that pit cells induce apoptosis in CC cells in vitro by the perforin/granzyme pathway.
Authors:
D Vermijlen; D Luo; B Robaye; C Seynaeve; M Baekeland; E Wisse
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Hepatology (Baltimore, Md.)     Volume:  29     ISSN:  0270-9139     ISO Abbreviation:  Hepatology     Publication Date:  1999 Jan 
Date Detail:
Created Date:  1999-02-03     Completed Date:  1999-02-03     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8302946     Medline TA:  Hepatology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  51-6     Citation Subset:  IM    
Affiliation:
Laboratory for Cell Biology and Histology, Free University of Brussels (VUB), Brussels, Belgium.dvemijl@cyto.vub.ac.be
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MeSH Terms
Descriptor/Qualifier:
Animals
Colonic Neoplasms / pathology*
Cytotoxicity, Immunologic*
DNA / chemistry,  isolation & purification
DNA Fragmentation*
Electrophoresis, Polyacrylamide Gel
Immunohistochemistry
Killer Cells, Natural / physiology*
Liver / cytology*,  immunology
Male
Membrane Glycoproteins / metabolism*
Microscopy, Electron
Perforin
Pore Forming Cytotoxic Proteins
Rats
Rats, Wistar
Serine Endopeptidases / metabolism*
Tumor Cells, Cultured
Chemical
Reg. No./Substance:
0/Membrane Glycoproteins; 0/Pore Forming Cytotoxic Proteins; 126465-35-8/Perforin; 9007-49-2/DNA; EC 3.4.21.-/Serine Endopeptidases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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