Linked Life Data

11358851

Source:http://linkedlifedata.com/resource/pubmed/id/11358851

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2001-5-18
pubmed:abstractText
Expression levels of gangliosides and glycosyltransferase genes responsible for their syntheses in human lung cancer cell lines and a normal bronchial epithelial cell line were analyzed. Both non-small cell lung cancers and small cell lung cancers (SCLCs) mainly expressed G(M2) and G(M1), whereas only SCLCs expressed b-series gangliosides, such as G(D2), G(D1b), and G(T1b). Accordingly, many SCLC cell lines showed up-regulation of the G(D3) synthase gene. Consequently, we introduced G(D3) synthase cDNA into a SCLC line with low expression of b-series gangliosides and analyzed the effects of newly expressed gangliosides on tumor phenotypes. The transfectant cells expressing high levels of G(D2) and G(D3) exhibited markedly increased growth rates and strongly enhanced invasion activities. Addition of anti-G(D2) monoclonal antibodies into the culture medium of these cells resulted in the marked growth suppression of G(D2)-expressing cell lines with reduced activation levels of mitogen-activated protein kinases but not of nonexpressants, suggesting that G(D2) plays important roles in cell proliferation. Moreover, G(D2)-expressing cells treated with anti-G(D2) antibodies showed features of apoptotic cell death at 30 min after addition of antibodies, i.e., shrinkage of cytoplasm, binding of Annexin V, and staining with propidium iodide, followed by DNA fragmentation. This G(D2)-mediated apoptosis was associated with caspase-3 activation and partly inhibited by a caspase inhibitor, z-Val-Ala-Asp-fluoromethyl ketone. The finding that anti-G(D2) antibodies suppressed the cell growth and induced apoptosis of SCLC cells strongly suggested the usefulness of G(D2) as a target for the therapy of disastrous cancer, although the precise mechanisms for apoptosis remain to be clarified.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4244-52
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11358851-Antibodies, Monoclonal, pubmed-meshheading:11358851-Apoptosis, pubmed-meshheading:11358851-Carbohydrate Sequence, pubmed-meshheading:11358851-Carcinoma, Small Cell, pubmed-meshheading:11358851-Cell Division, pubmed-meshheading:11358851-DNA, Complementary, pubmed-meshheading:11358851-Flow Cytometry, pubmed-meshheading:11358851-G(M1) Ganglioside, pubmed-meshheading:11358851-G(M2) Ganglioside, pubmed-meshheading:11358851-Gangliosides, pubmed-meshheading:11358851-Gene Expression Regulation, Enzymologic, pubmed-meshheading:11358851-Gene Expression Regulation, Neoplastic, pubmed-meshheading:11358851-Humans, pubmed-meshheading:11358851-Lung Neoplasms, pubmed-meshheading:11358851-Molecular Sequence Data, pubmed-meshheading:11358851-N-Acetylgalactosaminyltransferases, pubmed-meshheading:11358851-Phenotype, pubmed-meshheading:11358851-Sialyltransferases, pubmed-meshheading:11358851-Transfection, pubmed-meshheading:11358851-Up-Regulation
pubmed:year
2001
pubmed:articleTitle
Ganglioside G(D2) in small cell lung cancer cell lines: enhancement of cell proliferation and mediation of apoptosis.
pubmed:affiliation
Department of Biochemistry II, Nagoya University School of Medicine, 65 Tsurumai, Showa-ku, Nagoya 466-0065, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't