Peroxisome proliferator-activated receptor β expression in human breast epithelial cell lines of tumorigenic and non-tumorigenic origin

Suchanek, K. M.; May, Fiona J.; Lee, Won Jae; Holman, N. A.; Roberts‐Thomson, Sarah J.

doi:10.1016/s1357-2725(02)00025-0

Cited by 29 publications

(11 citation statements)

References 33 publications

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“…In mammary and hepatocellular cancers, PPARy activation stimulates cell proliferation and tumor growth (22,23). In addition, PPARy is overexpressed in human colorectal tumors (24), head and neck squamous carcinomas (25), endometrial adenocarcinomas (26), and human breast cancer cell lines (27). Although we have shown that activation of PPARy promotes intestinal tumor growth in mice, there is also evidence that its activation attenuates tumor growth (19)(20)(21)28).…”

Section: Introductionmentioning

confidence: 71%

Extracellular Signal-Regulated Kinase Is a Target of Cyclooxygenase-1-Peroxisome Proliferator-Activated Receptor-δ Signaling in Epithelial Ovarian Cancer

Daikoku¹,

Tranguch²,

Chakrabarty³

et al. 2007

Cancer Research

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The underlying causes of epithelial ovarian cancer (EOC) are unclear, and treatment options for patients with advanced disease are limited. There is evidence that the use of nonsteroidal anti-inflammatory drugs is associated with decreased risk of developing EOC. Nonsteroidal anti-inflammatory drugs inhibit cyclooxygenase (COX)-1 and COX-2, which catalyze prostaglandin biosynthesis. We previously showed that mouse and human EOCs have increased levels of COX-1, but not COX-2, and a COX-1-selective inhibitor, SC-560, attenuates prostaglandin production and tumor growth. However, the downstream targets of COX-1 signaling in EOC are not yet known. To address this question, we evaluated peroxisome proliferator-activated receptor D (PPARD) expression and function in EOC. We found that EOC cells express high levels of PPARD, and neutralizing PPARD function reduces tumor growth in vivo. More interestingly, aspirin, a nonsteroidal anti-inflammatory drug that preferentially inhibits COX-1, compromises PPARD function and cell growth by inhibiting extracellular signal-regulated kinases 1/2, members of the mitogen-activated protein kinase family. Our study, for the first time, shows that whereas PPARD can be a target of COX-1, extracellular signal-regulated kinase is a potential target of PPARD. The ability of aspirin to inhibit EOC growth in vivo is an exciting finding because of its low cost, lack of cardiovascular side effects, and availability. [Cancer Res 2007;67(11):5285-92]

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Section: Introductionmentioning

confidence: 71%

Extracellular Signal-Regulated Kinase Is a Target of Cyclooxygenase-1-Peroxisome Proliferator-Activated Receptor-δ Signaling in Epithelial Ovarian Cancer

Daikoku¹,

Tranguch²,

Chakrabarty³

et al. 2007

Cancer Research

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“…PPAR δ null macrophages exhibited loss of the dominant inhibitory effect by unliganded PPAR δ [60], which was previously identified by its ability to block PPAR α and PPAR γ transactivation through corepressor recruitment [60, 66, 67]. In breast cancer cells, PPAR δ expression was greater in ER − MDA-MB-231 breast cancer cells than in ER + MCF-7 cells [68], also suggesting a correlation with a more aggressive form of this disease. Indeed, tissue microarray analysis of invasive breast cancers indicated that PPAR δ is strongly expressed (see Figure 2, “+3”) in 52% of 164 samples, and thus may have value as a prognostic marker and therapeutic target.…”

Section: Pparδ Signalingmentioning

confidence: 99%

PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate

2008

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PPARγ and PPARδ agonists represent unique classes of drugs that act through their ability to modulate gene transcription associated with intermediary metabolism, differentiation, tumor suppression, and in some instances proliferation and cell adhesion. PPARγ agonists are used by millions of people each year to treat type 2 diabetes but may also find additional utility as relatively nontoxic potentiators of chemotherapy. PPARδ agonists produce complex actions as shown by their tumor promoting effects in rodents and their cholesterol-lowering action in dyslipidemias. There is now emerging evidence that PPARs regulate tumor suppressor genes and developmental pathways associated with transformation and cell fate determination. This review discusses the role of PPARγ and PPARδ agonists as modulators of these processes.

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“…This family of nuclear transcription factors comprises three isoforms (α, β/δ and γ) that bind fatty acids to regulate lipid metabolism and homeostasis but differ in target gene regulation. Both PPARα and PPARβ/δ have been shown to stimulate the proliferation of cancer cells [156,157] whereas a large body of evidence has shown that PPARγ is growth inhibitory [158][159][160]. Loss-of-function mutations in PPARγ have been associated with human colon cancer [161].…”

Section: Mechanism Of Action Of Pufas In Cancer Cellsmentioning

confidence: 99%

Dietary fat’gene interactions in cancer

Chen

Edwards

Kridel

et al. 2007

Cancer Metastasis Rev

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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.

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Peroxisome proliferator-activated receptor β expression in human breast epithelial cell lines of tumorigenic and non-tumorigenic origin

Cited by 29 publications

References 33 publications

Extracellular Signal-Regulated Kinase Is a Target of Cyclooxygenase-1-Peroxisome Proliferator-Activated Receptor-δ Signaling in Epithelial Ovarian Cancer

Extracellular Signal-Regulated Kinase Is a Target of Cyclooxygenase-1-Peroxisome Proliferator-Activated Receptor-δ Signaling in Epithelial Ovarian Cancer

PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate

Dietary fat’gene interactions in cancer

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