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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Regulation of dendritic cell genes by alpha fetoprotein

ABSTRACT: Human dendritic cells (DC) are suppressed by tumor-derived alpha fetoprotein (AFP), but less so by cord blood-derived normal AFP. We tested human DC from 5 healthy donors for transcriptional changes induced by tumor (tAFP) or cord blood (nAFP) AFP, vs. chicken ovalbumin (OVA) control.

ORGANISM(S): Homo sapiens

SUBMITTER: Lisa Butterfield

PROVIDER: E-GEOD-62005 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Tumor-derived α-fetoprotein impairs the differentiation and T cell stimulatory activity of human dendritic cells.

Pardee Angela D AD Shi Jian J Butterfield Lisa H LH

Journal of immunology (Baltimore, Md. : 1950) 20141029 11

Several tumor-derived factors have been implicated in dendritic cell (DC) dysfunction in cancer patients. α-fetoprotein (AFP) is an oncofetal Ag that is highly expressed in abnormalities of prenatal development and several epithelial cancers, including hepatocellular carcinoma (HCC). In HCC patients exhibiting high levels of serum AFP, we observed a lower ratio of myeloid/plasmacytoid circulating DCs compared with patients with low serum AFP levels and healthy donors. To test the effect of AFP o ...[more]

PMID: 25355916

Similar Datasets

Regulation of dendritic cell genes by alpha fetoprotein

Project description:Human dendritic cells (DC) are suppressed by tumor-derived alpha fetoprotein (AFP), but less so by cord blood-derived normal AFP.

2014-12-23 | GSE62005 | GEO

Glycosylation Profiling of Neoplastic Biomarker Alpha Fetoprotein Through Intact Mass Protein Analysis

Project description:Alpha fetoprotein (AFP) is a circulating cancer biomarker implicated in multiple neoplastic malignancies, including hepatocellular carcinoma (HCC). AFP glycoforms with core fucosylation structure (AFP-L3) are used clinically as a biomarker, to predict risk of developing HCC and to monitor its recurrence. Mature AFP has a single glycosylation site, while there is a high degree of structural variation in AFP-glycan modifications. Because AFP has single glycosylation site, masses of intact AFP proteoforms can be used to differentiate and identify PTM in their native states. We developed a method for intact AFP glycoform analysis that utilizes AFP-specific immune-enrichment, followed by LC-high resolution mass spectrometry (LC-HRMS) analysis to differentiate and quantitate the relative abundance of AFP glycoforms and evaluated the method’s performance.

2023-01-11 | PXD038606 | Pride

siRNA Administration Against AFP Inhibits Hepatocellular Carcinoma Proliferation in Vitro and Progression in Mice

Project description:Increased ?-fetoprotein (AFP) levels have been reported to predict a poor prognosis in hepatocellular carcinoma (HCC). We assessed the mechanism of AFP involvement in the progression of HCC and determined whether AFP could be a molecular target. We used human HCC cell lines to assess proliferation and apoptosis response to exogenous AFP. We introduced AFP small interfering RNA (siRNA) into HCC cell lines to examine whether it could inhibit cell proliferation and anti-apoptotic properties. The effects of systemically introduced AFP siRNA were assessed using a tumor xenotransplantation model. The effects of AFP on gene expression in HCC cell lines and human HCC specimens were examined. Exogenous AFP induced cell proliferation dose-dependently and inhibited apoptosis induced by 5-fluorouracil (5-FU) in all cell lines examined. AFP siRNA inhibited the proliferation of AFP-producing HCC cell lines and induced apoptosis in co-cultures with 5-FU. Tumor sizes in mice treated with AFP siRNA were significantly smaller than those in controls. AFP siRNA administration in mice induced a low proliferation index and a high apoptosis index in tumors. cDNA microarray analysis, reverse transcription-polymerase chain reaction (RT-PCR), and Western blot using HepG2 and HLE cells with AFP showed that AFP reduced expression of genes related to apoptosis (DFFB) and tumor suppression (NDRG2). Expression of these molecules was also suppressed in human HCC tissues that overexpress AFP. AFP is not only a passive tumor marker, but also an active tumor stimulator through several mechanisms. AFP siRNA introduction may be of possible therapeutic use for HCC. Keywords: Genetic modification Two-condition experiment, Control vs. AFP-stimulated cells.

2008-12-30 | E-GEOD-12307 | biostudies-arrayexpress

Glycosylation Profiling of Neoplastic Biomarker Alpha Fetoprotein Through Intact Mass Protein Analysis

Project description:Glycosylation is an important post-translational modification (PTM) mechanism of proteins, that modulates protein function. Measurement of clinically adopted cancer protein biomarkers is commonly performed using affinity-based techniques, which often suffer from poor specificity and inability to distinguish between closely related proteoforms. Alpha fetoprotein (AFP) is a circulating cancer biomarker implicated in multiple neoplastic malignancies, including hepatocellular carcinoma (HCC). AFP glycoforms with core fucosylation structure (AFP-L3) are used clinically as a biomarker, to predict risk of developing HCC and to monitor its recurrence. Mature AFP has a single glycosylation site, while there is a high degree of structural variation in AFP-glycan modifications. Because AFP has single glycosylation site, masses of intact AFP proteoforms can be used to differentiate and identify PTM in their native states. We developed a method for intact AFP glycoform analysis that utilizes AFP-specific immune-enrichment, followed by LC-high resolution mass spectrometry (LC-HRMS) analysis to differentiate and quantitate the relative abundance of AFP glycoforms and evaluated the method’s performance.

2023-01-11 | PXD038602 | Pride

Intact N-glycopeptides and proteomics from HCC tissue tumors with low and high AFP concentrations

Project description:Hepatocellular carcinoma (HCC) is still one of the malignant tumors with high morbidity and mortality in China and worldwide. Although AFP have been widely used as important biomarkers for HCC diagnosis and evaluation, the AFP level has a huge variation among HCC patient populations. Understanding the intrinsic heterogeneities of HCC associated with AFP levels is essential for the molecular mechanism studies of HCC with different AFP levels as well as for the potential early diagnosis and personalized treatment of HCC with AFP negative. Here, an integrated glycoproteomic and proteomic analysis of low and high AFP level of HCC tumors was performed to investigate the intrinsic heterogeneities of site-specific glycosylation associated with different AFP levels of HCC. we identified many commonly altered site-specific glycans from HCC tumors regardless of AFP levels, including decreased modifications by oligo-mannose and sialylated bi-antennary glycans, and increased modifications by bisecting glycans. By relative quantifying the intact glycopeptides between low and high AFP tumor groups, the great heterogeneities of site-specific N-glycans between two groups of HCC tumors were also uncovered. We found that several sialylated but not core fucosylated tri-antennary glycans were uniquely high-regulated in low AFP level of HCC tumors, while many core fucosylated bi-antennary or hybrid glycans as well as bisecting glycans were uniquely increased in high AFP tumors. The data provide a valuable resource for future HCC studies regarding the mechanism, heterogeneities and new biomarker discovery.

2020-03-19 | PXD016406 | Pride

Expression profiling of Notch constitutive activation in the liver of mice

Project description:Notch intracellular domain (NICD) is the active form of the Notch receptor. In this mouse model, NICD is inserted in the Rosa26 locus downstream of a loxP-STOP-LoxP (lsl) sequence and therefore NICD expression is dependant on Cre recombinase expression (Mono transgenic control Rosa26-lsl-NICD) . These mice are crossed with the AFP-Cre strain that expresses Cre in hepatoblasts due to its regulation by the AFP promoter and albumin enhancer (Double transgenic mutant AFP-Cre/Rosa26-lsl-NICD). Newborn mice at day 0 and day 2 are sacrificed and liver RNA samples from control monotransgenic Rosa26-lsl-NICD and from bitransgenic AFP-Cre/Rosa26-lsl-NICD (AFP-NICD) are obtained. Whole genome expression profiling of these samples is submitted. Five liver samples from Control mice and six liver samples from Mutant mice are analyzed using the Agilent Whole Mouse Genome Oligo Microarray G4122A platform. Array data was preprocessed and analyzed using GenePattern software and R.

2012-12-01 | E-GEOD-33560 | biostudies-arrayexpress

Expression data from tumor-associated endothelial cells of hepatocellular carcinoma

Project description:Primary uncultured CD31+ and CD105+ tumor endothelial cells (TEC), non-tumor endothelial cells (NEC) ,remnant cells from tumor (TC) and non-tumor liver tissue (NTC)of HCC tissues from patientswere isolated by magnetic-activated cell sorting. Affymetrix Human Gene ST Arrays were used to determine gene expression profiles of HCC cells and matched TEC and NEC cells. We use the gene expression profiling of the Human Genome U133 Plus 2.0 Arrays (Affymetrix, Santa Clara, CA) to identify distinct genes of TEC and NEC. Patient specimens were collected immediately after removal from patients with pathologically proven HCC and positive alpha-fetoprotein (AFP), then washed 3 times by phosphate buffer solution (PBS). Single cell suspension was obtained from separated tumor and non-tumor liver tissues of surgical specimens following the protocol (http://www.miltenyibiotec.com), then CD31+ cells or CD105+ cells were isolated using CD31 antibody or CD105 antibody conjugated magnetic beads in autoMACSpro (Meltenyi biotec).After the sample preparation, the gene expression profiling was performed using the Human Genome U133 Plus 2.0 Arrays (Affymetrix, Santa Clara, CA) according to manufacturerM-bM-^@M-^Ys protocols at ShanghaiBio Corporation (Shanghai, China).

2013-10-19 | E-GEOD-51401 | biostudies-arrayexpress

Expression profiling of Notch constitutive activation induced HCC in mice

Project description:Notch intracellular domain (NICD) is the active form of the Notch receptor. In this mouse model, NICD is inserted in the Rosa26 locus downstream of a loxP-STOP-LoxP (lsl) sequence and therefore NICD expression is dependant on Cre recombinase expression. These mice are crossed with the AFP-Cre strain that expresses Cre in hepatoblasts due to its regulation by the AFP promoter and albumin enhancer. Mice from 6 to 12 months are sacrificed and liver RNA samples from control monotransgenic Rosa26-lsl-NICD and confirmed HCC lesions from bitransgenic AFP-Cre/Rosa26-lsl-NICD (AFP-NICD) are obtained. Exon expression profiling of these samples are submitted. Four liver samples from monotransgenic mice (control) and five hepatocellular carcinoma samples from bitransgenic mice are analyzed using the Affymetrix GeneChip Mouse Gene 1.0 ST Array platform. Array data was preprocessed and analyzed using GenePattern software and R.

2012-12-01 | E-GEOD-33486 | biostudies-arrayexpress

Differential proteomics between AFP-negative HCC and adjacent non-tumor liver tissue

Project description:We screened and identified novel proteins in AFP-negative HCC tissue that were differentially expressed related to levels in adjacent non-tumor liver tissue using SWATH-MS proteome technology

2021-11-02 | PXD028854 | Pride

siRNA Administration Against AFP Inhibits Hepatocellular Carcinoma Proliferation in Vitro and Progression in Mice

Project description:Increased α-fetoprotein (AFP) levels have been reported to predict a poor prognosis in hepatocellular carcinoma (HCC). We assessed the mechanism of AFP involvement in the progression of HCC and determined whether AFP could be a molecular target. We used human HCC cell lines to assess proliferation and apoptosis response to exogenous AFP. We introduced AFP small interfering RNA (siRNA) into HCC cell lines to examine whether it could inhibit cell proliferation and anti-apoptotic properties. The effects of systemically introduced AFP siRNA were assessed using a tumor xenotransplantation model. The effects of AFP on gene expression in HCC cell lines and human HCC specimens were examined. Exogenous AFP induced cell proliferation dose-dependently and inhibited apoptosis induced by 5-fluorouracil (5-FU) in all cell lines examined. AFP siRNA inhibited the proliferation of AFP-producing HCC cell lines and induced apoptosis in co-cultures with 5-FU. Tumor sizes in mice treated with AFP siRNA were significantly smaller than those in controls. AFP siRNA administration in mice induced a low proliferation index and a high apoptosis index in tumors. cDNA microarray analysis, reverse transcription-polymerase chain reaction (RT-PCR), and Western blot using HepG2 and HLE cells with AFP showed that AFP reduced expression of genes related to apoptosis (DFFB) and tumor suppression (NDRG2). Expression of these molecules was also suppressed in human HCC tissues that overexpress AFP. AFP is not only a passive tumor marker, but also an active tumor stimulator through several mechanisms. AFP siRNA introduction may be of possible therapeutic use for HCC. Keywords: Genetic modification

2008-12-31 | GSE12307 | GEO

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