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Article ; Online: Polyunsaturated fatty acid metabolism in prostate cancer.

Berquin, Isabelle M / Edwards, Iris J / Kridel, Steven J / Chen, Yong Q

2011 Volume 30, Issue 3-4, Page(s) 295–309

Abstract: Polyunsaturated fatty acids (PUFA) play important roles in the normal physiology and in pathological states including inflammation and cancer. While much is known about the biosynthesis and biological activities of eicosanoids derived from ω6 PUFA, our ... ...

Abstract	Polyunsaturated fatty acids (PUFA) play important roles in the normal physiology and in pathological states including inflammation and cancer. While much is known about the biosynthesis and biological activities of eicosanoids derived from ω6 PUFA, our understanding of the corresponding ω3 series lipid mediators is still rudimentary. The purpose of this review is not to offer a comprehensive summary of the literature on fatty acids in prostate cancer but rather to highlight some of the areas where key questions remain to be addressed. These include substrate preference and polymorphic variants of enzymes involved in the metabolism of PUFA, the relationship between de novo lipid synthesis and dietary lipid metabolism pathways, the contribution of cyclooxygenases and lipoxygenases as well as terminal synthases and prostanoid receptors in prostate cancer, and the potential role of PUFA in angiogenesis and cell surface receptor signaling.
MeSH term(s)	Animals ; Dietary Fats, Unsaturated/metabolism ; Fatty Acids, Unsaturated/biosynthesis ; Fatty Acids, Unsaturated/metabolism ; Humans ; Lipid Metabolism ; Lipoxygenases/metabolism ; Male ; Neovascularization, Pathologic/metabolism ; Oxidation-Reduction ; Prostaglandin-Endoperoxide Synthases/metabolism ; Prostatic Neoplasms/blood supply ; Prostatic Neoplasms/enzymology ; Prostatic Neoplasms/metabolism ; Receptors, Prostaglandin/metabolism ; Signal Transduction
Chemical Substances	Dietary Fats, Unsaturated ; Fatty Acids, Unsaturated ; Receptors, Prostaglandin ; Lipoxygenases (EC 1.13.11.-) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1)
Language	English
Publishing date	2011-10-28
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1007/s10555-011-9299-7
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Article ; Online: Multi-targeted therapy of cancer by omega-3 fatty acids.

Berquin, Isabelle M / Edwards, Iris J / Chen, Yong Q

Cancer letters

2008 Volume 269, Issue 2, Page(s) 363–377

Abstract: Omega-3 (n-3) and omega-6 (n-6) polyunsaturated fatty acids (PUFAs) are essential fatty acids necessary for human health. Currently, the Western diet contains a disproportionally high amount of n-6 PUFAs and low amount of n-3 PUFAs, and the resulting ... ...

Abstract	Omega-3 (n-3) and omega-6 (n-6) polyunsaturated fatty acids (PUFAs) are essential fatty acids necessary for human health. Currently, the Western diet contains a disproportionally high amount of n-6 PUFAs and low amount of n-3 PUFAs, and the resulting high n-6/n-3 ratio is thought to contribute to cardiovascular disease, inflammation, and cancer. Studies in human populations have linked high consumption of fish or fish oil to reduced risk of colon, prostate, and breast cancer, although other studies failed to find a significant association. Nonetheless, the available epidemiological evidence, combined with the demonstrated effects of n-3 PUFAs on cancer in animal and cell culture models, has motivated the development of clinical interventions using n-3 PUFAs in the prevention and treatment of cancer, as well as for nutritional support of cancer patients to reduce weight loss and modulate the immune system. In this review, we discuss the rationale for using long-chain n-3 PUFAs in cancer prevention and treatment and the challenges that such approaches pose in the design of clinical trials.
MeSH term(s)	Animals ; Arachidonic Acid/metabolism ; Clinical Trials as Topic ; Eicosapentaenoic Acid/metabolism ; Fatty Acids, Omega-3/administration & dosage ; Fatty Acids, Omega-3/pharmacology ; Fatty Acids, Omega-6/administration & dosage ; Fatty Acids, Omega-6/pharmacology ; Humans ; Linoleic Acid/metabolism ; Lipid Peroxidation ; Neoplasms/drug therapy ; Neoplasms/prevention & control ; Nutritional Support ; alpha-Linolenic Acid/metabolism
Chemical Substances	Fatty Acids, Omega-3 ; Fatty Acids, Omega-6 ; alpha-Linolenic Acid (0RBV727H71) ; Arachidonic Acid (27YG812J1I) ; Linoleic Acid (9KJL21T0QJ) ; Eicosapentaenoic Acid (AAN7QOV9EA)
Language	English
Publishing date	2008-05-13
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2008.03.044
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Article: Omega-3 polyunsaturated fatty acids regulate syndecan-1 expression in human breast cancer cells.

Sun, Haiguo / Berquin, Isabelle M / Edwards, Iris J

Cancer research

2005 Volume 65, Issue 10, Page(s) 4442–4447

Abstract: Human epidemiologic studies and animal model studies support a role for n-3 polyunsaturated fatty acids (n-3 PUFA) in prevention or inhibition of breast cancer. However, mechanisms for this protection remain unclear. Syndecan-1 is a heparan sulfate ... ...

Abstract	Human epidemiologic studies and animal model studies support a role for n-3 polyunsaturated fatty acids (n-3 PUFA) in prevention or inhibition of breast cancer. However, mechanisms for this protection remain unclear. Syndecan-1 is a heparan sulfate proteoglycan, expressed on the surface of mammary epithelial cells and known to regulate many biological processes, including cytoskeletal organization, growth factor signaling, and cell-cell adhesion. We studied effects of n-3 PUFA on syndecan-1 expression in human mammary cell lines. PUFA were delivered to cells by low-density lipoproteins (LDL) isolated from the plasma of monkeys fed diets enriched in fish oil (n-3 PUFA) or linoleic acid (n-6 PUFA). Proteoglycan synthesis was measured by incorporation of [35S]-sodium sulfate. No effect of either LDL was observed in nontumorigenic MCF-10A cells, whereas in MCF-7 breast cancer cells, treatment with n-3-enriched LDL but not n-6-enriched LDL resulted in significantly greater synthesis of a proteoglycan identified by immunoprecipitation as syndecan-1. Using real-time reverse transcription-PCR (RT-PCR), it was shown that n-3-enriched LDL significantly increased the expression of syndecan-1 mRNA in a dose-dependent manner and maximal effective time at 8 hours of treatment. The effect was mimicked by an agonist for peroxisome proliferator-activated receptor gamma (PPARgamma) and eliminated by the presence of PPARgamma antagonist suggesting a role for PPARgamma in syndecan enhancement. Our studies show that n-3 LDL modifies the production of syndecan-1 in human breast cancer cells and suggest that biological processes regulated by syndecan-1 may be modified through LDL delivery of n-3 PUFA.
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Cercopithecus aethiops ; Fatty Acids, Omega-3/pharmacology ; Gene Expression/drug effects ; Humans ; Lipoproteins, LDL/pharmacology ; Membrane Glycoproteins/biosynthesis ; Membrane Glycoproteins/genetics ; PPAR gamma/physiology ; Proteoglycans/biosynthesis ; Proteoglycans/genetics ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Syndecan-1 ; Syndecans
Chemical Substances	Fatty Acids, Omega-3 ; Lipoproteins, LDL ; Membrane Glycoproteins ; PPAR gamma ; Proteoglycans ; RNA, Messenger ; SDC1 protein, human ; Syndecan-1 ; Syndecans
Language	English
Publishing date	2005-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-04-4200
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Article ; Online: Peroxisome proliferator-activated receptor gamma-mediated up-regulation of syndecan-1 by n-3 fatty acids promotes apoptosis of human breast cancer cells.

Sun, Haiguo / Berquin, Isabelle M / Owens, Rick T / O'Flaherty, Joseph T / Edwards, Iris J

Cancer research

2008 Volume 68, Issue 8, Page(s) 2912–2919

Abstract: Diets enriched in n-3 polyunsaturated fatty acids (n-3 PUFA) may protect against breast cancer but biochemical mechanisms are unclear. Our studies showed that the n-3 fatty acid docosahexaenoic acid (DHA) up-regulated syndecan-1 (SDC-1) in human breast ... ...

Abstract	Diets enriched in n-3 polyunsaturated fatty acids (n-3 PUFA) may protect against breast cancer but biochemical mechanisms are unclear. Our studies showed that the n-3 fatty acid docosahexaenoic acid (DHA) up-regulated syndecan-1 (SDC-1) in human breast cancer cells, and we tested the hypothesis that DHA-mediated up-regulation of SDC-1 induces apoptosis. DHA was delivered to MCF-7 cells by n-3 PUFA-enriched low-density lipoproteins (LDL) or by albumin in the presence or absence of SDC-1 small interfering RNA. The n-3 PUFA induced apoptosis, which was blocked by SDC-1 silencing. We also confirmed that SDC-1 up-regulation and apoptosis promotion by n-3 PUFA was mediated by peroxisome proliferator-activated receptor gamma (PPAR gamma). Using a luciferase gene driven by either a PPAR response element or a DR-1 site present in the SDC-1 promoter, reporter activities were enhanced by n-3 LDL, DHA, and PPAR gamma agonist, whereas activity of a luciferase gene placed downstream of a mutant DR-1 site was unresponsive. Cotransfection with dominant-negative PPAR gamma DNA eliminated the increase in luciferase activity. These data provide strong evidence that SDC-1 is a molecular target of n-3 PUFA in human breast cancer cells through activation of PPAR gamma and that n-3 PUFA-induced apoptosis is mediated by SDC-1. This provides a novel mechanism for the chemopreventive effects of n-3 PUFA in breast cancer.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Breast Neoplasms ; Cell Line, Tumor ; Chlorocebus aethiops ; Fatty Acids, Omega-3/pharmacology ; Female ; Fish Oils ; Humans ; PPAR gamma/physiology ; Polymerase Chain Reaction ; RNA, Neoplasm/genetics ; RNA, Neoplasm/isolation & purification ; Syndecan-1/genetics
Chemical Substances	Antineoplastic Agents ; Fatty Acids, Omega-3 ; Fish Oils ; PPAR gamma ; RNA, Neoplasm ; Syndecan-1
Language	English
Publishing date	2008-04-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-07-2305
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Article: Dietary fat-gene interactions in cancer.

Chen, Yong Q / Edwards, Iris J / Kridel, Steven J / Thornburg, Todd / Berquin, Isabelle M

Cancer metastasis reviews

2007 Volume 26, Issue 3-4, Page(s) 535–551

Abstract: Epidemiologic studies have suggested for decades an association between dietary fat and cancer risk. A large body of work performed in tissue culture and xenograft models of cancer supports an important role of various types of fat in modulating the ... ...

Abstract	Epidemiologic studies have suggested for decades an association between dietary fat and cancer risk. A large body of work performed in tissue culture and xenograft models of cancer supports an important role of various types of fat in modulating the cancer phenotype. Yet, the molecular mechanisms underlining the effects of fat on cancer initiation and progression are largely unknown. The relationships between saturated fat, polyunsaturated fat, cholesterol or phytanic acid with cancer have been reviewed respectively. However, few have considered the relationship between all of these fats and cancer. The purpose of this review is to present a more cohesive view of dietary fat-gene interactions, and outline a working hypothesis of the intricate connection between fat, genes and cancer.
MeSH term(s)	Animals ; Bile Acids and Salts/metabolism ; Cholesterol, Dietary/adverse effects ; Dietary Fats/adverse effects ; Fatty Acid Synthases/genetics ; Fatty Acids/administration & dosage ; Fatty Acids/biosynthesis ; Fatty Acids, Unsaturated/administration & dosage ; Humans ; Neoplasms/etiology ; Neoplasms/genetics ; Oxidation-Reduction ; PPAR gamma/metabolism ; Phytanic Acid/adverse effects ; Protein Prenylation ; Racemases and Epimerases/genetics ; Signal Transduction ; Vitamin D/therapeutic use
Chemical Substances	Bile Acids and Salts ; Cholesterol, Dietary ; Dietary Fats ; Fatty Acids ; Fatty Acids, Unsaturated ; PPAR gamma ; Vitamin D (1406-16-2) ; Phytanic Acid (14721-66-5) ; Fatty Acid Synthases (EC 2.3.1.85) ; Racemases and Epimerases (EC 5.1.-) ; alpha-methylacyl-CoA racemase (EC 5.1.99.4)
Language	English
Publishing date	2007-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1007/s10555-007-9075-x
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Article ; Online: Polyunsaturated fatty acids affect the localization and signaling of PIP3/AKT in prostate cancer cells.

Gu, Zhennan / Wu, Jiansheng / Wang, Shihua / Suburu, Janel / Chen, Haiqin / Thomas, Michael J / Shi, Lihong / Edwards, Iris J / Berquin, Isabelle M / Chen, Yong Q

Carcinogenesis

2013 Volume 34, Issue 9, Page(s) 1968–1975

Abstract: AKT is a serine-threonine protein kinase that plays important roles in cell growth, proliferation and apoptosis. It is activated after binding to phosphatidylinositol phosphates (PIPs) with phosphate groups at positions 3,4 and 3,4,5 on the inositol ring. ...

Abstract	AKT is a serine-threonine protein kinase that plays important roles in cell growth, proliferation and apoptosis. It is activated after binding to phosphatidylinositol phosphates (PIPs) with phosphate groups at positions 3,4 and 3,4,5 on the inositol ring. In spite of extensive research on AKT, one aspect has been largely overlooked, namely the role of the fatty acid chains on PIPs. PIPs are phospholipids composed of a glycerol backbone with fatty acids at the sn-1 and sn-2 position and inositol at the sn-3 position. Here, we show that polyunsaturated fatty acids (PUFAs) modify phospholipid content. Docosahexaenoic acid (DHA), an ω3 PUFA, can replace the fatty acid at the sn-2 position of the glycerol backbone, thereby changing the species of phospholipids. DHA also inhibits AKT(T308) but not AKT(S473) phosphorylation, alters PI(3,4,5)P3 (PIP3) and phospho-AKT(S473) protein localization, decreases pPDPK1(S241)-AKT and AKT-BAD interaction and suppresses prostate tumor growth. Our study highlights a potential novel mechanism of cancer inhibition by ω3 PUFA through alteration of PIP3 and AKT localization and affecting the AKT signaling pathway.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Fatty Acids, Omega-3/administration & dosage ; Fatty Acids, Omega-3/metabolism ; Fatty Acids, Unsaturated/administration & dosage ; Fatty Acids, Unsaturated/metabolism ; Humans ; Male ; Mice ; Mice, Transgenic ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects
Chemical Substances	Fatty Acids, Omega-3 ; Fatty Acids, Unsaturated ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67)
Language	English
Publishing date	2013-04-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgt147
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Zs.A 1558: Show issues

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Article: Expression signature of the mouse prostate.

Berquin, Isabelle M / Min, Younong / Wu, Ruping / Wu, Hong / Chen, Yong Q

The Journal of biological chemistry

2005 Volume 280, Issue 43, Page(s) 36442–36451

Abstract: Genetically engineered mice are being used increasingly for delineating the molecular mechanisms of prostate cancer development. Epithelium-stroma interactions play a critical role in prostate development and tumorigenesis. To better understand gene ... ...

Abstract	Genetically engineered mice are being used increasingly for delineating the molecular mechanisms of prostate cancer development. Epithelium-stroma interactions play a critical role in prostate development and tumorigenesis. To better understand gene expression patterns in the normal sexually mature mouse prostate, epithelium and stroma were laser-capture microdissected from ventral, dorsolateral, and anterior prostate lobes. Genome-wide expression was measured by DNA microarrays. Our analysis indicated that the gene expression pattern in the mouse dorsolateral lobe was closest to that of the human prostate peripheral zone, supporting the hypothesis that these prostate compartments are functionally equivalent. Stroma from a given lobe had closer gene expression patterns with stroma from other lobes than epithelium from the same lobe. Stroma appeared to have higher expression complexity than epithelium. Specifically, stromal cells had higher expression levels of genes implicated in cell adhesion, muscle development, and contraction, in structural constituents of cytoskeleton and actin binding, and in components such as sarcomere and extracellular matrix collagen. Among the genes that were enriched in the epithelium were secretory proteins, including seminal vesicle protein secretion 2 and 5. Surprisingly, prostate stroma expressed many osteogenic molecules, as confirmed by immunohistochemistry. A "bone-like" environment in the prostate may predispose prostate cells for survival in the bone. Chemokine Cxcl12 but not its receptor, Cxcr4, was expressed in normal prostate. In prostate tumors, interestingly, Cxcl12 was up-regulated in epithelial cells with a concomitant expression of Cxcr4. Expression of both the receptor and ligand may provide an autocrine mechanism for tumor cell migration and invasion.
MeSH term(s)	Actins/metabolism ; Animals ; Cell Adhesion ; Cell Movement ; Cell Survival ; Chemokine CXCL12 ; Chemokines, CXC/metabolism ; Chromosome Mapping ; Collagen/metabolism ; Cytoskeleton/metabolism ; Epithelium/metabolism ; Extracellular Matrix/metabolism ; Gene Expression Regulation ; Gene Expression Regulation, Neoplastic ; Genetic Engineering ; Genome ; Immunohistochemistry ; Lasers ; Ligands ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muscle Contraction ; Neoplasm Invasiveness ; Oligonucleotide Array Sequence Analysis ; Prostate/metabolism ; Prostatic Neoplasms/metabolism ; Receptors, CXCR4/metabolism ; Sarcomeres/metabolism ; Tissue Distribution ; Up-Regulation
Chemical Substances	Actins ; CXCL12 protein, human ; Chemokine CXCL12 ; Chemokines, CXC ; Cxcl12 protein, mouse ; Ligands ; Receptors, CXCR4 ; Collagen (9007-34-5)
Language	English
Publishing date	2005-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M504945200
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Article: In vivo and in vitro regulation of syndecan 1 in prostate cells by n-3 polyunsaturated fatty acids.

Edwards, Iris J / Sun, Haiguo / Hu, Yunping / Berquin, Isabelle M / O'Flaherty, Joseph T / Cline, J Mark / Rudel, Lawrence L / Chen, Yong Q

The Journal of biological chemistry

2008 Volume 283, Issue 26, Page(s) 18441–18449

Abstract: Syndecan 1 is the major proteoglycan produced by epithelial cells. It is strategically localized at the plasma membrane to participate in growth factor signaling and cell-cell and cell-matrix interactions. Its expression may modulate the properties of ... ...

Abstract	Syndecan 1 is the major proteoglycan produced by epithelial cells. It is strategically localized at the plasma membrane to participate in growth factor signaling and cell-cell and cell-matrix interactions. Its expression may modulate the properties of epithelial lineage tumor cells in which it is generally down-regulated compared with nontumor progenitors. The present study examined the regulation of syndecan 1 in prostate epithelial cells by n-3 polyunsaturated fatty acids. In prostate tissue of mice, syndecan 1 immunostaining was demonstrated in epithelial cells throughout each gland. In animals fed an n-3 polyunsaturated fatty acid-enriched diet, syndecan 1 mRNA was increased in all prostate glands. In the human prostate cancer cell line, PC-3, delivery of exogenous n-3 (but not n-6) fatty acids resulted in up-regulation of syndecan 1 expression. This effect was mimicked by a peroxisome proliferator-activated receptor (PPAR) gamma agonist, troglitazone, and inhibited in the presence of a PPARgamma antagonist and in cells transfected with dominant negative PPARgamma cDNA. Using a luciferase gene driven either by a PPAR response element or by a DR-1 site present in the syndecan 1 promoter, reporter activation was increased by n-3 low density lipoprotein, docosahexaenoic acid, and troglitazone, whereas activity of a luciferase gene placed downstream of a mutant DR-1 site was unresponsive. These findings indicate that syndecan 1 is up-regulated by n-3 fatty acids by a transcriptional pathway involving PPARgamma. This mechanism may contribute to the chemopreventive properties of n-3 fatty acids in prostate cancer.
MeSH term(s)	Animals ; Cell Line, Tumor ; Chromans/pharmacology ; Fatty Acids, Omega-3/metabolism ; Gene Expression Regulation ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Mice ; PPAR gamma/agonists ; PPAR gamma/antagonists & inhibitors ; Promoter Regions, Genetic ; Prostate/metabolism ; RNA, Messenger/metabolism ; Syndecan-1/biosynthesis ; Syndecan-1/genetics ; Thiazolidinediones/pharmacology ; Tissue Distribution ; Troglitazone
Chemical Substances	Chromans ; Fatty Acids, Omega-3 ; PPAR gamma ; RNA, Messenger ; Syndecan-1 ; Thiazolidinediones ; Troglitazone (I66ZZ0ZN0E)
Language	English
Publishing date	2008-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M802107200
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Article: Y-box-binding protein 1 confers EGF independence to human mammary epithelial cells.

Berquin, Isabelle M / Pang, Bing / Dziubinski, Michele L / Scott, Latanya M / Chen, Yong Q / Nolan, Garry P / Ethier, Stephen P

Oncogene

2005 Volume 24, Issue 19, Page(s) 3177–3186

Abstract: The epidermal growth factor receptor (EGFR) is linked to poor outcome in breast cancer, and resistance to hormonal therapy is often accompanied by activation of growth factor receptors. To investigate the mechanism(s) by which EGFR becomes activated in ... ...

Abstract	The epidermal growth factor receptor (EGFR) is linked to poor outcome in breast cancer, and resistance to hormonal therapy is often accompanied by activation of growth factor receptors. To investigate the mechanism(s) by which EGFR becomes activated in breast cancer, we screened a cDNA expression library for genes that mediate EGF-independent proliferation of human mammary epithelial cells (HMECs). We isolated the NSEP1 cDNA encoding Y-box-binding protein 1 (YB-1), a multifunctional transcriptional and translational regulator. This cDNA conferred growth factor independence to HMECs. YB-1-transduced cells overexpressed EGFR, but ErbB-2 (Her-2/neu) levels were unchanged. Moreover, EGFR was constitutively phosphorylated in the absence of exogenous ligand. In these cells, an EGFR-blocking antibody failed to inhibit proliferation, conditioned medium activity could not be detected, and the synthesis of EGFR ligands was reduced compared to parental cells. This suggests that EGFR is activated in a ligand-independent fashion. However, cell growth could be blocked with an ErbB kinase inhibitor, indicating that EGFR signaling plays a major role in YB-1-induced growth factor independence. Taken together, our results demonstrate that YB-1 overexpression can induce EGF independence in HMECs via activation of the EGFR pathway. This could represent one of the mechanisms by which YB-1 contributes to breast tumor aggressiveness.
MeSH term(s)	Alleles ; Blotting, Northern ; Breast/metabolism ; Breast Neoplasms/metabolism ; CCAAT-Enhancer-Binding Proteins/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Cells, Cultured ; Cloning, Molecular ; DNA, Complementary/metabolism ; Epidermal Growth Factor/metabolism ; Epithelial Cells/metabolism ; Gene Library ; Humans ; Immunoblotting ; Immunoprecipitation ; Ligands ; Microscopy, Fluorescence ; NFI Transcription Factors ; Neoplasm Invasiveness ; Phosphorylation ; Protein Biosynthesis ; Receptor, Epidermal Growth Factor/metabolism ; Receptor, ErbB-2/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Time Factors ; Transcription Factors/metabolism ; Transcription, Genetic ; Y-Box-Binding Protein 1
Chemical Substances	CCAAT-Enhancer-Binding Proteins ; DNA, Complementary ; Ligands ; NFI Transcription Factors ; Transcription Factors ; Y-Box-Binding Protein 1 ; Epidermal Growth Factor (62229-50-9) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2005-04-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/sj.onc.1208504
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Zs.A 2218: Show issues

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Article ; Online: Decorin suppresses prostate tumor growth through inhibition of epidermal growth factor and androgen receptor pathways.

Hu, Yunping / Sun, Haiguo / Owens, Rick T / Wu, Jiansheng / Chen, Yong Q / Berquin, Isabelle M / Perry, Donna / O'Flaherty, Joseph T / Edwards, Iris J

Neoplasia (New York, N.Y.)

2009 Volume 11, Issue 10, Page(s) 1042–1053

Abstract: Epidermal growth factor receptor (EGFR) and androgen receptor (AR) pathways play pivotal roles in prostate cancer progression. Therefore, agents with dual-targeting ability may have important therapeutic potential. Decorin, a proteoglycan present in the ... ...

Abstract	Epidermal growth factor receptor (EGFR) and androgen receptor (AR) pathways play pivotal roles in prostate cancer progression. Therefore, agents with dual-targeting ability may have important therapeutic potential. Decorin, a proteoglycan present in the tumor microenvironment, is known to regulate matrix assembly, growth factor binding, and receptor tyrosine kinase activity. Here, we show that in prostate-specific Pten(P-/-) mice, a genetically defined, immune-competent mouse model of prostate cancer, systemic delivery of decorin inhibits tumor progression by targeting cell proliferation and survival pathways. Moreover, in human prostate cancer cells, we show that decorin specifically inhibits EGFR and AR phosphorylation and cross talk between these pathways. This prevents AR nuclear translocation and inhibits the production of prostate specific antigen. Further, the phosphatidylinositol-3 kinase (PI3K)/Akt cell survival pathway is suppressed leading to tumor cell apoptosis. Those findings highlight the effectiveness of decorin in the presence of a powerful genetic cancer risk and implicate decorin as a potential new agent for prostate cancer therapy by targeting EGFR/AR-PI3K-Akt pathways.
MeSH term(s)	Animals ; Blotting, Western ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Proliferation/drug effects ; Decorin ; Epidermal Growth Factor/metabolism ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Extracellular Matrix Proteins/pharmacology ; Humans ; Immunohistochemistry ; Male ; Mice ; Mice, Knockout ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation/drug effects ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Protein Transport/drug effects ; Proteoglycans/genetics ; Proteoglycans/metabolism ; Proteoglycans/pharmacology ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; Receptor Cross-Talk/drug effects ; Receptors, Androgen/metabolism ; Signal Transduction/drug effects
Chemical Substances	DCN protein, human ; Dcn protein, mouse ; Decorin ; Extracellular Matrix Proteins ; Proteoglycans ; Receptors, Androgen ; Epidermal Growth Factor (62229-50-9) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; ErbB Receptors (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67)
Language	English
Publishing date	2009-09-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1593/neo.09760
Database	MEDical Literature Analysis and Retrieval System OnLINE

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