Linked Life Data

19932628

Source:http://linkedlifedata.com/resource/pubmed/id/19932628

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-3-24
pubmed:abstractText
It is known that all-trans retinoic acid (RA) is a useful therapeutic anticancer agent in breast cancer that acts by inducing apoptosis and growth inhibition. Insulin-like growth factor-I (IGF-I) is also known to be a growth hormone that plays an important role in cell proliferation and apoptosis. We examined the relationships between RA-induced protein kinase C (PKC)-delta, the secretion and synthesis of IGF-I, and oxidative stress. RA at 10(-8)M and 10(-7)M increased PKC-delta phosphorylation (the ratio of phosphorylated to total PKC-delta) (p<0.05) and decreased the secretion and synthesis of IGF-I (p<0.05) compared to control, with the effects peaking for treatment with 10(-7)M RA for 72h. The silencing of PKC-delta prevented the RA-induced inhibition of the secretion and synthesis of IGF-I and cell viability (p<0.05). Application of 10(-7)M RA for 72h increased the level of thiobarbituric-acid-reactive substances and the expression of inducible nitric oxide synthase relative to control (p<0.05). These increases were blocked by suppressing PKC-delta and by pretreatment with the antioxidants glutathione and diphenyleneiodonium (p<0.05). These antioxidants also reversed the RA-induced inhibition of the secretion and synthesis of IGF-I and cell viability to control levels (p<0.05). The effects of suppressing IGF-I demonstrate that IGF-I plays a critical role in the RA-induced inhibition of the cell viability. These results indicate that the anticancer effects of RA are mediated by inhibition of the secretion and synthesis of IGF-I, and involve a PKC-delta-dependent mechanism, and they provide evidence of an interaction between PKC-delta and reactive oxygen species.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1532-2238
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2009 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-9
pubmed:meshHeading
pubmed-meshheading:19932628-Antineoplastic Agents, pubmed-meshheading:19932628-Breast Neoplasms, pubmed-meshheading:19932628-Cell Line, Tumor, pubmed-meshheading:19932628-Cell Survival, pubmed-meshheading:19932628-Dose-Response Relationship, Drug, pubmed-meshheading:19932628-Enzyme Activation, pubmed-meshheading:19932628-Female, pubmed-meshheading:19932628-Gene Expression Regulation, pubmed-meshheading:19932628-Humans, pubmed-meshheading:19932628-Insulin-Like Growth Factor I, pubmed-meshheading:19932628-Oxidative Stress, pubmed-meshheading:19932628-Phosphorylation, pubmed-meshheading:19932628-Protein Kinase C-delta, pubmed-meshheading:19932628-Reactive Oxygen Species, pubmed-meshheading:19932628-Time Factors, pubmed-meshheading:19932628-Tretinoin, pubmed-meshheading:19932628-Up-Regulation
pubmed:year
2010
pubmed:articleTitle
Oxidative stress in MCF-7 cells is involved in the effects of retinoic acid-induced activation of protein kinase C-delta on insulin-like growth factor-I secretion and synthesis.
pubmed:affiliation
Department of Veterinary Physiology, College of Veterinary Medicine, Chonbuk National University, Duk-Jin Dong 1 Ga 664-14, Jeonju City, Chonbuk, South Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't