Linked Life Data

11687965

Source:http://linkedlifedata.com/resource/pubmed/id/11687965

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
47
pubmed:dateCreated
2001-10-31
pubmed:abstractText
Despite many efforts to alter the relentlessly aggressive progression of tumors of neural origin, individuals bearing these tumors exhibit poor prognosis for long-term survival. In an attempt to find an effective treatment, we examined the efficacy of the non-steroidal anti-inflammatory drug, flurbiprofen, to suppress the growth of tumor cell lines derived from medulloblastoma and glioblastoma multiforme. Results from cell proliferation assays have revealed that flurbiprofen effectively inhibits the growth of various tumor cells in a dose-dependent manner and causes a noticeable change in the progression of cells through cell cycle stages. Treatment of tumor cells with flurbiprofen reduced the number of cells in G1 and G2, and significantly increased their numbers in S phase, suggesting that, flurbiprofen accelerates G1/S entry, and/or delays cell exit from S to G2/M stages. Results from RNase protection assay and Western blot analysis showed that while treatment of cells with flurbiprofen causes a minor change in the RNA level of different cyclins, there is a significant decrease in the level of cyclin B protein upon flurbiprofen treatment. Examination of tumor suppressors by RNase protection technique showed a subtle increase in the levels of several tumor suppressors upon flurbiprofen treatment. Interestingly, at the protein level, p53 tumor suppressor was substantially increased upon flurbiprofen treatment, yet the level of p21, a downstream target for p53 remained unchanged. Curiously, treatment of the cells with flurbiprofen enhanced the level of COX-2 expression. Results from co-immunoprecipitation showed association of COX-2 with p53 in tumor cells. These observations suggest that the interaction of COX-2 with p53 may cause p21-independent suppression of tumor cell growth upon flurbiprofen treatment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6864-70
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11687965-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:11687965-Brain Neoplasms, pubmed-meshheading:11687965-Cell Cycle, pubmed-meshheading:11687965-Cell Division, pubmed-meshheading:11687965-Cyclin B, pubmed-meshheading:11687965-Cyclooxygenase 2, pubmed-meshheading:11687965-Flurbiprofen, pubmed-meshheading:11687965-Genes, Tumor Suppressor, pubmed-meshheading:11687965-Glioblastoma, pubmed-meshheading:11687965-Humans, pubmed-meshheading:11687965-Isoenzymes, pubmed-meshheading:11687965-Kinetics, pubmed-meshheading:11687965-Medulloblastoma, pubmed-meshheading:11687965-Membrane Proteins, pubmed-meshheading:11687965-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:11687965-RNA, Neoplasm, pubmed-meshheading:11687965-Tumor Cells, Cultured, pubmed-meshheading:11687965-Tumor Suppressor Protein p53
pubmed:year
2001
pubmed:articleTitle
Inhibition of human brain tumor cell growth by the anti-inflammatory drug, flurbiprofen.
pubmed:affiliation
Laboratory of Cancer Biology and Intervention, Center for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, Philadelphia, Pennsylvania, PA 19122, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.