Linked Life Data

1319775

Source:http://linkedlifedata.com/resource/pubmed/id/1319775

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1992-8-6
pubmed:abstractText
We compared tumor necrosis factor (TNF) metabolism by wild-type MCF-7 (WT) cells, by 40-fold doxorubicin resistant (40F) breast cancer cells and by PC3 and LNCaP prostate cancer cell lines. MCF-7 WT and LNCaP cell lines were sensitive to TNF cytotoxicity and both lines produced two major intracellular TNF degradation products of 15 kDa and 5.5 kDa. The MCF-7 40F and the PC3 cell lines were resistant to TNF and produced multiple TNF degradation products with molecular weights lower than 15 kDa. Both the breast and prostate lines showed TNF receptor crosslinking patterns consistent with a molecular weight of 55 kDa. The breast and LNCaP lines expressed TNF receptors with an apparent dissociation constant (Kd) of 0.4 to 0.6 nM, while the TNF resistant line had a Kd of 2 nM. Similar receptor numbers per cell were found for all cell types (4,000 to 8,000/cell), and comparable levels of TNF internalization were noted. TNF-conditioned medium from the TNF-sensitive cell types was cytotoxic toward both the TNF-sensitive and TNF-resistant lines, and the toxicity was significantly blocked by an anti-TNF monoclonal antibody. Hydrophobic interaction column HPLC fractionation of the TNF-degradation products produced by MCF-7 WT and LNCaP cells revealed that the trimeric, monomeric, and 5.5 kDa fractions possessed the greatest in vitro antitumor activity. These findings suggest that a TNF degradation product, produced selectively by TNF-sensitive cells, may contribute to the antitumor action of TNF.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0965-0407
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
91-101
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:1319775-Antibodies, Monoclonal, pubmed-meshheading:1319775-Breast Neoplasms, pubmed-meshheading:1319775-Cell Division, pubmed-meshheading:1319775-Cytotoxicity, Immunologic, pubmed-meshheading:1319775-Doxorubicin, pubmed-meshheading:1319775-Drug Resistance, pubmed-meshheading:1319775-Electrophoresis, pubmed-meshheading:1319775-Female, pubmed-meshheading:1319775-Gene Expression, pubmed-meshheading:1319775-Humans, pubmed-meshheading:1319775-Iodine Radioisotopes, pubmed-meshheading:1319775-Male, pubmed-meshheading:1319775-Oncogenes, pubmed-meshheading:1319775-Prostatic Neoplasms, pubmed-meshheading:1319775-RNA, Messenger, pubmed-meshheading:1319775-Receptor, Epidermal Growth Factor, pubmed-meshheading:1319775-Receptors, Cell Surface, pubmed-meshheading:1319775-Receptors, Tumor Necrosis Factor, pubmed-meshheading:1319775-Recombinant Proteins, pubmed-meshheading:1319775-Tumor Cells, Cultured, pubmed-meshheading:1319775-Tumor Necrosis Factor-alpha
pubmed:year
1992
pubmed:articleTitle
Selective formation of tumor necrosis factor-alpha (TNF) degradation products contributes to TNF mediated cytotoxicity.
pubmed:affiliation
Section of Biochemical and Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
pubmed:publicationType
Journal Article, Comparative Study