Prostaglandin E2 Regulates the Complement Inhibitor CD55/Decay-accelerating Factor in Colorectal Cancer

Holla, Vijaykumar; Wang, Dingzhi; Brown, Joanne R.; Mann, Jason R.; Katkuri, Sharada; DuBois, Raymond N.

doi:10.1074/jbc.m407403200

Cited by 56 publications

(40 citation statements)

References 57 publications

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“…An affect H. pylori-induced IL-8 production, 3 a response that has previously been shown to be dependent on MAPK signaling (44). Therefore, these findings are not consistent with a model of DAF autoregulation in H. pyloriinfected gastric epithelial cells.…”

Section: Discussioncontrasting

confidence: 55%

“…Although the mechanism through which NOD1 induces activation of p38 remains unclear (56), there are several mechanisms by which p38 may promote increased DAF expression. Activation of p38 can transactivate the transcription factor CREB, which has previously been shown to transcriptionally up-regulate DAF in intestinal epithelial cells (41,42,44). Alternatively, daf mRNA transcript stability has been shown to be increased by activation of p38 in monocytic cell lines (57).…”

Section: Discussionmentioning

confidence: 99%

“…The daf promoter contains a B response element, and activation of NF-B leads to the up-regulation of DAF in response to proinflammatory stimuli (41)(42)(43)(44). To define the role of NF-B in H. pylori-induced DAF expression, MKN28 cells were transiently transfected with constructs that express either a dominant-negative IB␣ or dominant-negative IB kinase ␤ as well as a NF-B-responsive luciferase reporter construct.…”

Section: H Pylori Induction Of Daf Occurs Via a Nf-b-independentmentioning

confidence: 99%

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Regulation of the Helicobacter pylori Cellular Receptor Decay-accelerating Factor

O’Brien

Romero–Gallo

Schneider³

et al. 2008

Journal of Biological Chemistry

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Chronic gastritis induced by Helicobacter pylori is the strongest known risk factor for peptic ulceration and distal gastric cancer, and adherence of H. pylori to gastric epithelial cells is critical for induction of inflammation. One H. pylori constituent that increases disease risk is the cag pathogenicity island, which encodes a secretion system that translocates bacterial effector molecules into host cells. Decay-accelerating factor (DAF) is a cellular receptor for H. pylori and a mediator of the inflammatory response to this pathogen. H. pylori induces DAF expression in human gastric epithelial cells; therefore, we sought to define the mechanism by which H. pylori up-regulates DAF and to extend these findings into a murine model of H. pylori-induced injury. Co-culture of MKN28 gastric epithelial cells with the wild-type H. pylori cag ؉ strain J166 induced transcriptional expression of DAF, which was attenuated by disruption of a structural component of the cag secretion system (cagE). H. pylori-induced expression of DAF was dependent upon activation of the p38 mitogen-activated protein kinase pathway but not NF-B. Hypergastrinemic INS-GAS mice infected with wildtype H. pylori demonstrated significantly increased DAF expression in gastric epithelium versus uninfected controls or mice infected with an H. pylori cagE ؊ isogenic mutant strain. These results indicate that H. pylori cag ؉ strains induce up-regulation of a cognate cellular receptor in vitro and in vivo in a cag-dependent manner, representing the first evidence of regulation of an H. pylori host receptor by the cag pathogenicity island.

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Section: Discussioncontrasting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Section: H Pylori Induction Of Daf Occurs Via a Nf-b-independentmentioning

confidence: 99%

See 1 more Smart Citation

Regulation of the Helicobacter pylori Cellular Receptor Decay-accelerating Factor

O’Brien

Romero–Gallo

Schneider³

et al. 2008

Journal of Biological Chemistry

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“…COX-2/PGE 2 signaling plays critical roles in neoangiogenesis; homozygous deletion of EP 2 R significantly reduces the number and size of intestinal polyps in APC ⌬716 mice that is associated with a reduction of VEGF expression, suggesting that PGE 2 /EP 2 signaling is critical for increased levels of VEGF in intestinal neoplasm (19 4 receptors are coupled to stimulatory G (G s ) proteins and signal through increased cAMP, whereas the EP 3 R is coupled to inhibitory G (G i ) proteins which inhibit the generation of cAMP. PGE 2 stimulates the transcription of a number of genes through the cAMP/PKA pathway where the cAMP responsive element (CRE) within the promoter plays critical roles (13,41). The CRE consists of an 8-bp palindrome (TGACGTCA) and is typically found within 100 nt of the TATA box.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Induces the Expression of IL-1α in Colon Cancer Cells

Shao

Sheng

2007

The Journal of Immunology

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PGE2 has been shown to exert pro-oncogenic effects in colorectal neoplasia through producing autocrine or paracrine growth factors. In the present study, we demonstrate that PGE2 induced the expression of IL-1α in colon cancer cells, which plays critical roles in tumor metastasis and neoangiogenesis in a variety of cancers. PGE2 increased the levels of both IL-1α mRNA and protein, suggesting a positive feedback loop between the IL-1 pathway and PGE2 signaling. Mechanistically, PGE2 induced the expression of IL-1α at both transcriptional and posttranscriptional levels. PGE2 stimulated the transcriptional activity of the IL-1α promoter and significantly stabilized IL-1α mRNA. Moreover, we show that IL-1α enhanced colorectal neoplasia, stimulating cell migration and neoangiogenesis. Knockdown of the expression of IL-1α by small-interfering RNA resulted in a reduction of vascular endothelial growth factor secretion in colon cancer cells and an inhibition of tube formation by HUVECs. Thus, our results suggest that PGE2 induces the expression of proinflammatory cytokine IL-1α, which may potentially enhance the proneoplastic actions of the cyclooxygenase-2/PGE2 signaling pathway.

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“…53 The Mut construct was generated by sitedirected mutagenesis using the QuickChange kit (Stratagene, La Jolla, CA, USA) to mutate the C at c.-198 to G using the WT DAF promoter construct as a template. The mutant sequence was verified using an ABI Prism 3100 automated sequencer before further evaluation.…”

Section: Plasmid Constructsmentioning

confidence: 99%

A functional SNP in the regulatory region of the decay-accelerating factor gene associates with extraocular muscle pareses in myasthenia gravis

et al. 2009

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Complement activation in myasthenia gravis (MG) may damage muscle endplate and complement regulatory proteins such as decay-accelerating factor (DAF) or CD55 may be protective. We hypothesize that the increased prevalence of severe extraocular muscle (EOM) dysfunction among African MG subjects reported earlier may result from altered DAF expression. To test this hypothesis, we screened the DAF gene sequences relevant to the classical complement pathway and found an association between myasthenics with EOM paresis and the DAF regulatory region c.-198C4G SNP (odds ratio ¼ 8.6; P ¼ 0.0003). This single nucleotide polymorphism (SNP) results in a twofold activation of a DAF 5 0 -flanking region luciferase reporter transfected into three different cell lines. Direct matching of the surrounding SNP sequence within the DAF regulatory region with the known transcription factor-binding sites suggests a loss of an Sp1-binding site. This was supported by the observation that the c.-198C4G SNP did not show the normal lipopolysaccharide-induced DAF transcriptional upregulation in lymphoblasts from four patients. Our findings suggest that at critical periods during autoimmune MG, this SNP may result in inadequate DAF upregulation with consequent complement-mediated EOM damage. Susceptible individuals may benefit from anti-complement therapy in addition to immunosuppression.

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Prostaglandin E2 Regulates the Complement Inhibitor CD55/Decay-accelerating Factor in Colorectal Cancer

Cited by 56 publications

References 57 publications

Regulation of the Helicobacter pylori Cellular Receptor Decay-accelerating Factor

Regulation of the Helicobacter pylori Cellular Receptor Decay-accelerating Factor

Prostaglandin E2 Induces the Expression of IL-1α in Colon Cancer Cells

A functional SNP in the regulatory region of the decay-accelerating factor gene associates with extraocular muscle pareses in myasthenia gravis

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