Thus, RXR-selective retinoids that inhibit AP-1 activity and suppress COX-2 expression may be particularly promising drugs for breast cancer prevention.
To investigate the effects of cyclooxygenase-2 (COX-2) overexpression on breast cancer development, we stably transfected MCF-10F human breast epithelial cells with an expression vector containing human COX-2 cDNA oriented in the sense (10F-S) or antisense (10F-AS) direction.
This review focuses on the molecular targeting compounds directed against the known molecular pathways involved in breast cancer such as: type I growth factors (HER-2/neu; epidermal growth factor receptor [EGFR]), angiogenesis, cyclooxigenase-2 (COX-2) and farnesylation.
Cyclooxygenase-2 (COX-2) overexpression is a widely recognized feature of human breast cancer and inhibitors of the enzyme have antitumor effects in a subset of tumor settings.
To determine whether COX-2 induces drug resistance, plasmids encoding the COX-2 gene were stably transfected into ERalpha-positive MCF-7 human breast cancer cells (MCF-7/COX-2).
Two COX-2 overexpressing human breast cancer cell lines (Her-18 and MDA-MB-436) were treated with celecoxib (20 micromol/L and 50 micromol/L) and Ad-mda7 (multiplicity of infection, 1000 and 2000 viral particles/cell).
In a human breast cancer xenograft model, dietary administration of curcumin significantly decreased the incidence of breast cancer metastasis to the lung and suppressed the expression of NF-kappaB, cyclooxygenase 2, and matrix metalloproteinase-9.
Quantitative analysis of aromatase mRNA expression derived from various promoters (I.4, I.3, PII and I.7) and its association with expression of TNF-alpha, IL-6 and COX-2 mRNAs in human breast cancer.
Higher levels of COX-2 isoform were observed in breast cancer tissue when compared to normal breast tissue, and a strong association between CYP19 gene expression and the expression of COX genes are found.
Study of COX-2, Ki67, and p53 expression to predict effectiveness of 5-flurouracil, epirubicin and cyclophosphamide with celecoxib treatment in breast cancer patients.
Studies have shown higher levels of COX-2 isoform in breast cancer tissue when compared to normal breast tissue, and this is accompanied by high concentrations of prostaglandin E(2) (PGE(2)).
Prostaglandin E(2) plays a growth-stimulatory role in breast cancer, and the rate-limiting enzyme in its synthesis, cyclooxygenase-2, is often overexpressed in these cancers.
We present data suggesting that inhibiting COX-2 activity in vivo regulates IDO expression within the tumor microenvironment; this is further corroborated in the MDA-MB-231 human breast cancer cell line.