Document Detail


Conjugated linoleic acid inhibits proliferation and induces apoptosis of normal rat mammary epithelial cells in primary culture.
MedLine Citation:
PMID:  10388518     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The trace fatty acid conjugated linoleic acid (CLA) inhibits rat mammary carcinogenesis when fed prior to carcinogen during pubertal mammary gland development or during the promotion phase of carcinogenesis. The following studies were done to investigate possible mechanisms of these effects. Using a physiological model for growth and differentiation of normal rat mammary epithelial cell organoids (MEO) in primary culture, we found that CLA, but not linoleic acid (LA), inhibited growth of MEO and that this growth inhibition was mediated both by a reduction in DNA synthesis and a stimulation of apoptosis. The effects of CLA did not appear to be mediated by changes in epithelial protein kinase C (PKC) since neither total activity nor expression nor localization of PKC isoenzymes alpha, beta II, delta, epsilon, eta, or zeta were altered in the epithelium of CLA-fed rats. In contrast, PKCs delta, epsilon, and eta were specifically upregulated and associated with a lipid-like, but acetone-insoluble, fibrillar material found exclusively in adipocytes from CLA-fed rats. Taken together, these observations demonstrate that CLA can act directly to inhibit growth and induce apoptosis of normal MEO and may thus prevent breast cancer by its ability to reduce mammary epithelial density and to inhibit the outgrowth of initiated MEO. Moreover, the changes in mammary adipocyte PKC expression and lipid composition suggest that the adipose stroma may play an important in vivo role in mediating the ability of CLA to inhibit mammary carcinogenesis.
Authors:
M M Ip; P A Masso-Welch; S F Shoemaker; W K Shea-Eaton; C Ip
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Experimental cell research     Volume:  250     ISSN:  0014-4827     ISO Abbreviation:  Exp. Cell Res.     Publication Date:  1999 Jul 
Date Detail:
Created Date:  1999-08-25     Completed Date:  1999-08-25     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0373226     Medline TA:  Exp Cell Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  22-34     Citation Subset:  IM    
Copyright Information:
Copyright 1999 Academic Press.
Affiliation:
Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York, 14263, USA. mip@sc3101.med.buffalo.edu
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / drug effects,  metabolism
Animals
Anticarcinogenic Agents / metabolism,  pharmacology*
Apoptosis / drug effects*
Cell Differentiation / drug effects
Cell Division / drug effects
Cells, Cultured
Cytoplasm / metabolism
DNA / biosynthesis
Dietary Fats / metabolism
Epithelial Cells / drug effects
Female
Isoenzymes / metabolism
Isomerism
Linoleic Acids / metabolism,  pharmacology*
Linoleic Acids, Conjugated*
Mammary Glands, Animal / cytology*,  drug effects
Mice
Organoids / drug effects
Protein Kinase C / metabolism
Protein Kinase C-delta
Protein Kinase C-epsilon
Rabbits
Rats
Rats, Sprague-Dawley
Grant Support
ID/Acronym/Agency:
CA 16056/CA/NCI NIH HHS; CA 61763/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Anticarcinogenic Agents; 0/Dietary Fats; 0/Isoenzymes; 0/Linoleic Acids; 0/Linoleic Acids, Conjugated; 1839-11-8/9,11-linoleic acid; 9007-49-2/DNA; EC 2.7.1.-/Prkcd protein, mouse; EC 2.7.1.-/Prkcd protein, rat; EC 2.7.1.-/Prkce protein, mouse; EC 2.7.1.-/Prkce protein, rat; EC 2.7.1.-/protein kinase C eta; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.13/Protein Kinase C-delta; EC 2.7.11.13/Protein Kinase C-epsilon

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