Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:4.1.1.17 (
ornithine decarboxylase
)
6,351
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Caffeic acid phenethyl ester
(
CAPE
) was isolated from propolis (a product of honeybee hives) that has been used in folk medicine as a potent antiinflammatory agent.
CAPE
is cytotoxic to tumor and virally transformed but not to normal cells. Our main goal was to establish whether
CAPE
inhibits the tumor promoter (12-O-tetradecanoylphorbol-13-acetate)-induced processes associated with carcinogenesis. Topical treatment of SENCAR mice with very low doses (0.1-6.5 nmol/topical treatment) of
CAPE
strongly inhibits the following 12-O-tetradecanoylphorbol-13-acetate-mediated oxidative processes that are considered essential for tumor promotion: (a) polymorphonuclear leukocyte infiltration into mouse skin and ears, as quantified by myeloperoxidase activity; (b) hydrogen peroxide (H2O2) production; and (c) formation of oxidized bases in epidermal DNA, as measured by 5-hydroxymethyluracil and 8-hydroxylguanine. A 0.5-nmol dose of
CAPE
suppresses the oxidative burst of human polymorphonuclear leukocytes by 50%. At higher doses (1-10 mumol),
CAPE
inhibits edema and
ornithine decarboxylase
induction in CD-1 and SENCAR mice. Interestingly, we discovered that 12-O-tetradecanoylphorbol-13-acetate-induced H2O2 production in bovine lenses also is inhibited by
CAPE
. Cumulatively, these findings point to
CAPE
as being a potent chemopreventive agent, which may be useful in combating diseases with strong inflammatory and/or oxidative stress components, i.e., various types of cancer and possibly cataract development.
...
PMID:Inhibition of tumor promoter-mediated processes in mouse skin and bovine lens by caffeic acid phenethyl ester. 768 Feb 81
Caffeic acid phenethyl ester
(
CAPE
) was evaluated for its potential in regulating keratinocyte proliferation.
CAPE
inhibited the proliferation of SV40 transformed keratinocytes (Z114) in a concentration- and time-dependent manner. Inhibition by
CAPE
was seen with 0.5 to 5.0 micrograms/ml at 48 h. Cell toxicity was observed at 10 micrograms/ml by changes in morphology and decreased viability. Pretreatment of Z114 cells with
CAPE
significantly prevented the full induction of
ornithine decarboxylase
(
ODC
) by epidermal growth factor (EGF) in a concentration- and time-dependent manner. Inhibition was observed with a concentration of
CAPE
as low as 1 microgram/ml, and complete inhibition of
ODC
induction by EGF occurred at 5 micrograms/ml. Northern analysis showed that treatment of cells with
CAPE
for 24 h suppressed EGF induction of
ODC
gene expression. Incubation of Z114 cells with
CAPE
for 24 h resulted in a concentration-dependent decrease in EGF binding and a 30% reduction in the EGF induced autophosphorylation of the EGF receptor.
CAPE
decreased both membranous and cytosolic PKC activity in a concentration- and time-dependent manner. Because significant inhibition of keratinocyte proliferation occurred at concentrations of
CAPE
that interfered with PKC activity and EGF signal transduction but did not cause overt toxicity,
CAPE
may prove useful for the treatment of hyperproliferative skin diseases.
...
PMID:Caffeic acid phenethyl ester inhibits proliferation of human keratinocytes and interferes with the EGF regulation of ornithine decarboxylase. 883 88
