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Impact of Ino-C2-PAF on the gene expression profile of HaCaT cells after stimulation with pro-inflammatory cytokines

ABSTRACT: New alkyl-phospholipids (APLs) that are structurally derived from the platelet-activating factor are promising candidates for anticancer treatment. After the incorporation into cell membranes, APLs are able to interfere with a wide variety of key enzymes implicated in cell growth, motility, invasion and apoptosis. Recently, using Agilent cDNA microarray technology, we could demonstrate that the glycosidated APL Ino-C2-PAF inhibited the expression of several genes associated with immune response and inflammation in immortalized keratinocytes HaCaT. Here, we analyzed the impact of Ino-C2-PAF on the gene expression profile of HaCaT cells treated with several pro-inflammatory cytokines (IL-1α, IL-17, IL-22, TNF-α and oncostatin-M).

ORGANISM(S): Homo sapiens

PROVIDER: GSE37361 | GEO | 2013/01/01

SECONDARY ACCESSION(S): PRJNA159561

REPOSITORIES: GEO

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Impact of Ino-C2-PAF on the gene expression profile of HaCaT cells after stimulation with pro-inflammatory cytokines

Project description:New alkyl-phospholipids (APLs) that are structurally derived from the platelet-activating factor are promising candidates for anticancer treatment. After the incorporation into cell membranes, APLs are able to interfere with a wide variety of key enzymes implicated in cell growth, motility, invasion and apoptosis. Recently, using Agilent cDNA microarray technology, we could demonstrate that the glycosidated APL Ino-C2-PAF inhibited the expression of several genes associated with immune response and inflammation in immortalized keratinocytes HaCaT. Here, we analyzed the impact of Ino-C2-PAF on the gene expression profile of HaCaT cells treated with several pro-inflammatory cytokines (IL-1M-NM-1, IL-17, IL-22, TNF-M-NM-1 and oncostatin-M). The influence of Ino-C2-PAF on the transcriptional profile of immortalized keratinocytes (HaCaT) was analyzed treating HaCaT cells with 5 M-BM-5M Ino-C2-PAF in the presence of a mixture of pro-inflammatory cytokines (IL-1M-NM-1, IL-17, IL-22, TNF-M-NM-1 and oncostatin-M) for 24 h. Control cells were left untreated. Three independent experiments were performed for each condition, except for control cells where only two experiments were performed. Control cells were mainly necessary to demonstrate the efficiency of this in vitro inflammation model for keratinocytes.

2013-01-01 | E-GEOD-37361 | biostudies-arrayexpress

Influence of alkyl-phospholipids on the gene expression profile of immortalized keratinocytes HaCaT

Project description:New alkyl-phospholipids (APLs) that are structurally derived from the platelet-activating factor are promising candidates for anticancer treatment. After the incorporation into cell membranes, APLs are able to interfere with a wide variety of key enzymes implicated in cell growth, motility, invasion and apoptosis. Besides the prototype edelfosine, we presented a novel group of APLs, glycosidated phospholipids that efficiently inhibit cell proliferation. Two members of this group, Ino-C2-PAF and Glc-PAF, display high efficacy and low cytotoxicity in immortalized non-tumorigenic skin keratinocyte cell line HaCaT. However, the influence of APLs on the transcription of the whole genome is still unknown. Here, using Agilent cDNA microarray technology, we compared global gene expression profiles of HaCaT cells treated with edelfosine, Ino-C2-PAF or Glc-PAF with the profile of control cells. The influence of APLs on the transcriptional profile of immortalized keratinocytes (HaCaT) was analyzed treating HaCaT cells with respectively 5 M-BM-5M Ino-C2-PAF, Glc-PAF and edelfosine for 24 h. Control cells were left untreated. Three independent experiments were performed for each condition.

2011-03-01 | E-GEOD-20722 | biostudies-arrayexpress

Influence of alkyl-phospholipids on the gene expression profile of immortalized keratinocytes HaCaT

2011-03-01 | GSE20722 | GEO

Platelet activating factor (PAF) promotes immunosuppressive neutrophil differentiation within tumors

Project description:Chronic inflammatory milieu in the tumor microenvironment (TME) leads to the recruitment and differentiation of myeloid-derived suppressor cells (MDSCs). Polymorphonuclear (PMN)-MDSCs, which are phenotypically and morphologically defined as a subset of neutrophils, cause major immune suppression in the TME, posing a significant challenge in the development of effective immunotherapies. Despite recent advances in our understanding of PMN-MDSC functions, the mechanism that gives rise to immunosuppressive neutrophils within the TME remains elusive. Both in vivo and in vitro, newly recruited neutrophils into the tumor sites remained activated and highly motile for several days and developed immunosuppressive phenotypes, as indicated by increased arginase 1 (Arg1) and dcTrail-R1 expression and suppressed anti-cancer CD8 T cell cytotoxicity. The strong suppressive function was successfully recapitulated by incubating naïve neutrophils with cancer cell culture supernatant in vitro. Cancer metabolite secretome analyses of the culture supernatant revealed that both murine and human cancers released lipid mediators to induce the differentiation of immunosuppressive neutrophils. Liquid chromatography–mass spectrometry (LC-MS) lipidomic analysis identified platelet activation factor (PAF; 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) as a common tumor-derived lipid mediator that induces neutrophil differentiation. Lysophosphatidylcholine acyltransferase 2 (LPCAT2), the PAF biosynthetic enzyme, is upregulated in human pancreatic ductal adenocarcinoma (PDAC) and shows an unfavorable correlation with patient survival across multiple cancer types. Our study identifies PAF as a novel lipid-driven mechanism of MDSC differentiation in the TME, providing a potential target for cancer immunotherapy.

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