Linked Life Data

1372531

Source:http://linkedlifedata.com/resource/pubmed/id/1372531

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1992-4-28
pubmed:abstractText
TPA (12-O-tetradecanoylphorbol-13-acetate), a potent tumor promoter, has been shown to stimulate or inhibit cell growth depending on the cell type investigated. We recently found that RT101 cells, a transformed mouse JB6 epidermal cell line, acquired a greater growth inhibition response to TPA during conventional subcultivation. The growth of low-passage RT101 cells was slightly inhibited by TPA in monolayer culture but stimulated in soft agar. In contrast, the growth of high-passage cells was greatly inhibited by TPA in both monolayer culture and in soft agar. Inhibition was dose dependent, directly correlated with protein kinase C-activating activities of tumor promoters, and was found to be reversible. TPA-treated high-passage cells were greatly reduced in volume, showed extensive abnormal mitoses, and were more susceptible to detachment. High-passage cells were also found to be less tumorigenic as indicated by in vivo tumorigenicity assay in nude mice. TPA treatment rendered cells still less tumorigenic in the case of both cell lines. The mechanism for acquisition of increased sensitivity to TPA of RT101 cells during subculture was investigated; it involved nonrandom DNA damage and detachment of nonviable cells. The results suggest the possibility that early-passage RT101 cells contained two subpopulations, one TPA-sensitive and one TPA-resistant population. Conventional subcultivation may have selected for the former subpopulation. The sensitive subpopulation may have been irreversibly inhibited as a result of TPA-induced cell killing, possibly apoptosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
52
pubmed:geneSymbol
fos, jun
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1907-15
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1372531-Animals, pubmed-meshheading:1372531-Benzoyl Peroxide, pubmed-meshheading:1372531-Catalase, pubmed-meshheading:1372531-Cell Division, pubmed-meshheading:1372531-Cell Line, Transformed, pubmed-meshheading:1372531-DNA, pubmed-meshheading:1372531-DNA Damage, pubmed-meshheading:1372531-Epidermal Growth Factor, pubmed-meshheading:1372531-Genes, fos, pubmed-meshheading:1372531-Genes, jun, pubmed-meshheading:1372531-Glutathione Peroxidase, pubmed-meshheading:1372531-Lyngbya Toxins, pubmed-meshheading:1372531-Mice, pubmed-meshheading:1372531-Mice, Nude, pubmed-meshheading:1372531-Neoplasm Transplantation, pubmed-meshheading:1372531-RNA, pubmed-meshheading:1372531-Superoxide Dismutase, pubmed-meshheading:1372531-Tetradecanoylphorbol Acetate, pubmed-meshheading:1372531-Tumor Necrosis Factor-alpha
pubmed:year
1992
pubmed:articleTitle
Acquisition of a growth-inhibitory response to phorbol ester involves DNA damage.
pubmed:affiliation
Biological Carcinogenesis and Development Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.