Signal Transducer and Activator of Transcription 3 Activates CCAAT Enhancer-binding Protein δ Gene Transcription in G0Growth-arrested Mouse Mammary Epithelial Cells and in Involuting Mouse Mammary Gland

Hutt, Julie A.; O'Rourke, John P.; DeWille, James W.

doi:10.1074/jbc.m004476200

Cited by 72 publications

(91 citation statements)

References 47 publications

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“…Importantly, we identified targets that have been previously reported as Stat3 targets in the literature. These include upregulated genes such as fibrinogen, lipopolysaccharide-binding protein (LBP), SOCS3, c/EBPd, BCL6, JunB, and Myc (Fujitani et al, 1994;Schumann et al, 1996;Hutt et al, 2000;Reljic et al, 2000;Bowman et al, 2001;Duan and SimpsonHaidaris, 2003;He et al, 2003). These putative Stat3-regulated genes were then grouped into distinct known biological functions of the encoded proteins, including apoptosis, cell cycle, cell signaling, invasion, and inflammation.…”

Section: Identification Of Stat3-regulated Genes Using Oligonucleotidmentioning

confidence: 99%

Stat3 regulates genes common to both wound healing and cancer

et al. 2005

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Section: Identification Of Stat3-regulated Genes Using Oligonucleotidmentioning

confidence: 99%

Stat3 regulates genes common to both wound healing and cancer

et al. 2005

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“…Nuclear extracts from U937 cells were prepared, and electrophoretic mobility shift/antibody interference assays were performed as described previously (50). Complementary pairs of site-specific methylated and unmethylated oligonucleotides were from Integrated DNA Technologies-TEMA Ricerca (Bologna, Italy).…”

Section: Electrophoretic Mobility Shift Assays and Antibody Interferementioning

confidence: 99%

Eicosapentaenoic Acid Demethylates a Single CpG That Mediates Expression of Tumor Suppressor CCAAT/Enhancer-binding Protein δ in U937 Leukemia Cells

Ceccarelli

Racanicchi

Martelli

et al. 2011

Journal of Biological Chemistry

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Polyunsaturated fatty acids (PUFAs) inhibit proliferation and induce differentiation in leukemia cells. To investigate the molecular mechanisms whereby fatty acids affect these processes, U937 leukemia cells were conditioned with stearic, oleic, linolenic, ␣-linolenic, arachidonic, eicosapentaenoic, and docosahexaenoic acids. PUFAs affected proliferation; eicosapentaenoic acid (EPA) was the most potent on cell cycle progression. EPA enhanced the expression of the myeloid lineage-specific transcription factors CCAAT/enhancer-binding proteins (C/EBP␤ and C/EBP␦), PU.1, and c-Jun, resulting in increased expression of the monocyte lineage-specific target gene, the macrophage colony-stimulating factor receptor. Indeed, it is known that PU.1 and C/EBPs interact with their consensus sequences on a small DNA fragment of macrophage colony-stimulating factor receptor promoter, which is a determinant for expression. We demonstrated that C/EBP␤ and C/EBP␦ bind the same response element as a heterodimer. We focused on the enhanced expression of C/EBP␦, which has been reported to be a tumor suppressor gene silenced by promoter hypermethylation in U937 cells. After U937 conditioning with EPA and bisulfite sequencing of the ؊370/؊20 CpG island on the C/EBP␦ promoter region, we found a site-specific CpG demethylation that was a determinant for the binding activity of Sp1, an essential factor for C/EBP␦ gene basal expression. Our results provide evidence for a new role of PUFAs in the regulation of gene expression. Moreover, we demonstrated for the first time that re-expression of the tumor suppressor C/EBP␦ is controlled by the methylation state of a site-specific CpG dinucleotide.

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“…The IL-6 upregulation of C/EBP in mammary epithelium (Hutt et al 2000) and HepG2 cells (Yamada et al 1997) has been shown to be mediated by the 115 to 98 region of the promoter, but our data indicated that this site was not sensitive to LIF regulation in adipocytes (Fig. 6).…”

Section: Figurementioning

confidence: 38%

“…We also demonstrated that LIF increased C/EBP expression after an acute exposure. We have identified three LIF-responsive sites in the C/EBP promoter that are distinct from the previously reported STAT3 binding site for IL-6 regulation in mammary epithelial cells (Hutt et al 2000) and hepatocytes (Yamada et al 1997). Moreover, these three newly identified and LIF-responsive sites bind STAT1, rather than STAT3.…”

Section: Figurementioning

confidence: 64%

“…The role of STAT3 in the upregulation of C/EBP has been investigated in other cell types, and evidence indicated that the 115 to 98 site in the C/EBP promoter was bound by STAT3 following stimulation with interleukin (IL)-6 (Yamada et al 1997, Hutt et al 2000. Hence, we examined the ability of LIF to induce binding to the 115 to 98 element of the C/EBP promoter.…”

Section: Resultsmentioning

confidence: 99%

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Effects of leukemia inhibitory factor on 3T3-L1 adipocytes

Hogan¹,

Stephens

2005

Journal of Endocrinology

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Leukemia inhibitory factor (LIF) is a member of the gp130 cytokine family and signals through the receptor complex of gp130 and the LIF receptor (LIFR) to activate the JAK/STAT signaling cascade. Since LIF activates STATs 1 and 3 in adipocytes, we examined the effects of LIF on 3T3-L1 adipocytes. Our studies clearly demonstrate that LIF treatment had minimal effects on adipocyte differentiation as judged by marker gene expression, but did inhibit triacylglyceride (TAG) accumulation during adipogenesis. Acute treatment with LIF resulted in increased expression of suppressors of cytokine signaling-3 (SOCS3) and CCAAT/enhancer-binding protein-(C/EBP ) mRNA in 3T3-L1 adipocytes. Moreover, the upregulation of C/EBP correlated with binding to three sites in the C/EBP promoter by LIF-activated protein complexes that contained STAT1 and not STAT3. Chronic treatment with LIF resulted in decreased protein levels of sterol regulatory element binding protein-1 (SREBP1) and fatty acid synthase (FAS), but had no effect on the expression of other adipocyte marker proteins or on TAG levels in mature 3T3-L1 adipocytes. LIF had a small effect on insulin-stimulated glucose uptake in 3T3-L1 adipocytes, but did not cause insulin resistance following chronic treatment. These findings indicate that LIF has similar and distinct effects in comparison with the effects of other gp130 cytokines on cultured fat cells. In summary, our results support a role for LIF in the regulation of proteins involved in lipid synthesis and in the modulation of signal transduction pathways in 3T3-L1 adipocytes.

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Signal Transducer and Activator of Transcription 3 Activates CCAAT Enhancer-binding Protein δ Gene Transcription in G0Growth-arrested Mouse Mammary Epithelial Cells and in Involuting Mouse Mammary Gland

Cited by 72 publications

References 47 publications

Stat3 regulates genes common to both wound healing and cancer

Stat3 regulates genes common to both wound healing and cancer

Eicosapentaenoic Acid Demethylates a Single CpG That Mediates Expression of Tumor Suppressor CCAAT/Enhancer-binding Protein δ in U937 Leukemia Cells

Effects of leukemia inhibitory factor on 3T3-L1 adipocytes

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