Down-regulation of C/EBPalpha in breast cancer cells by hypoxia-estrogen combination is mainly due to hypoxia.

CCAAT/enhancer binding protein-alpha (C/EBPalpha) is involved in the control of cell differentiation and proliferation. It has been previously shown that hypoxia (H) down-regulates C/EBPalpha in breast cancer cells; here the effect of estrogen (E(2)) during H on C/EBPalpha in T-47D cell line was examined. By quantitative RT-PCR the C/EBPalpha mRNA stability was analyzed at 21% O(2) and 1% O(2) under E(2).

Hypoxia down-regulates CCAAT/enhancer binding protein-alpha expression in breast cancer cells.

The transcription factor CCAAT/enhancer binding protein-alpha (C/EBP alpha) is involved in the control of cell differentiation and proliferation, and has been suggested to act as a tumor suppressor in several cancers. By using microarray analysis, we have previously shown that hypoxia and estrogen down-regulate C/EBP alpha mRNA in T-47D breast cancer cells. Here, we have examined the mechanism by which the down-regulation by hypoxia takes place.

Hypoxia and estrogen co-operate to regulate gene expression in T-47D human breast cancer cells.

Experimental and clinical studies have shown that both estrogen (E2) and hypoxia (H) are involved in tumor development and progression. A study was undertaken to determine whether these factors could interact to modulate gene expression using a microarray approach. We screened the transcript levels of over 8000 genes in the estrogen receptor (ERalpha) positive T-47D human breast cancer cell lines maintained at 21% O2 or 1% O2 with or without E2 co-treatment.

Peroxisome proliferator-activated receptor-gamma down-regulates chondrocyte matrix metalloproteinase-1 via a novel composite element.

Interleukin-1beta (IL-1beta) induces degradation via hyperexpression of an array of genes, including metalloproteinases (MMP), in cartilage cells during articular degenerative diseases. In contrast, natural ligands for peroxisome proliferator-activated receptors (PPARs) display protective anti-cytokine effects in these cells. We used the PPAR agonist rosiglitazone (Rtz) to investigate PPAR-gamma isotype on IL-1beta-target genes.

Basic fibroblast growth factor as a selective inducer of matrix Gla protein gene expression in proliferative chondrocytes.

Matrix Gla protein (MGP) is a member of the vitamin K-dependent gamma carboxylase protein family expressed in cartilage. Insulin-like growth factor I (IGF1) stimulates chondrocyte differentiation, whereas basic fibroblast growth factor (FGF2) acts in an opposite manner. We explored the differential expression and regulation by IGF1 and FGF2 of the MGP gene during chondrocyte differentiation.