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GSE28406
Homo sapiens
16 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Pluripotent stem cells, including human embryonic stem (hES) and induced pluripotent stem (hiPS) cells, have been regarded as useful sources for cell?based transplantation therapy. However immunogenicity of the cells remains the major determinant for successful clinical application. We report the examination of several hES cell lines (NTU1 and H9), hiPS cell lines, and their derivatives (including stem cell?derived hepatocytes) for the expression of major histocompatibility complex (MHC), natural killer (NK) cell receptor (NKp30, NKp44, NKp46) ligand, immune?related genes, human leukocyte antigen (HLA) haplotyping, and the effects in functional mixed lymphocyte reaction (MLR). Flow cytometry showed lower levels (percentages and fluorescence intensities) of MHC class I (MHC?I) molecules, 2?microglobulin and HLA?E in undifferentiated stem cells, but the levels were increased after co?treatment with interferon gamma and/or in vitro differentiation. Antigen presenting cell markers (CD11c, CD80 and CD86) and MHC?II (HLA?DP, DQ and DR) remained low throughout the treatments. Recognitions of stem cells/derivatives by NK lysis receptors were lower or absent. Activation of responder lymphocytes was significantly lower by undifferentiated stem cells than by allogeneic lymphocytes in MLR, but differentiated NTU1 hES cells induced a cell number?dependent lymphocyte proliferation comparable with that by allogeneic lymphocytes. Interestingly activation of lymphocytes by differentiated hiPS cells or H9 cells became blunted at higher cell numbers. Real?time RT?PCR showed significant differential expression of immune privilege genes (TGF?2, Arginase 2, Indole 1, GATA3, POMC, VIP, CALCA, CALCB, IL?1RN, CD95L, CR1L, Serpine 1, HMOX1, IL6, LGALS3, HEBP1, THBS1, CD59 and LGALS1) in pluripotent stem cells/derivatives when compared to somatic cells. It is concluded that pluripotent stem cells/derivatives are predicted to be immunogenic, though evidences suggest some levels of potential immune privilege. In addition, differential immunogenicity may exist between different pluripotent stem cell lines and their derivatives
Publication Title
Characteristic expression of major histocompatibility complex and immune privilege genes in human pluripotent stem cells and their derivatives.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
TBR1 is a forebrain specific T-box transcription factor. Tbr1-/- mice have been characterized by defective axonal projections from cerebral cortex and abnormal neuronal migration of cerebral cortex and amygdala.
Publication Title
Tbr1 haploinsufficiency impairs amygdalar axonal projections and results in cognitive abnormality.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 7 Downloadable Samples
Illumina HiSeq 4000
Description
We performed RNA-Seq analysis of wildtype and three EPAS1-/- 786-O single cell clones generated by CRISPR/Cas9 to identify the HIF-2a-responsive genes in this cell line. Samples from wildtype 786-O cells treated with DMSO or HIF-2a antagonist compound C2 were also included in this analysis. Overall design: In this experiment, we analyzed the transcriptomic profiles of 2 replicates of wildtype (WT) EPAS1+/+ 786-O cells, 1 replicate for each of the three independent EPAS1-/- 786-O single cell clones, 1 replicate of WT-786-O cells treated with DMSO and 1 replicate of WT-786-O cells treated with 10uM HIF-2a antagonist C2.
Publication Title
A GPX4-dependent cancer cell state underlies the clear-cell morphology and confers sensitivity to ferroptosis.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 18 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip (gene symbol), Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Sorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.
Publication Title
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Sorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.
Publication Title
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Sorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.
Publication Title
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 15 Downloadable Samples
- Ion Torrent Proton
Description
Tumor-infiltrating macrophages, NK cells, CD8+ and CD4+ T cells sorted from clear cell renal cell carcinoma patient specimens. Overall design: 4 macrophage samples (CD45+CD3-CD56-CD14+), 2 CD16+ NK cell samples (CD45+CD3-CD56+CD16+), 5 CD8+ T cell samples (CD45+CD3+CD8+), 3 CD4+ T cell samples (CD45+CD3+CD4+), and one non-immune cell sample (CD45-).
Publication Title
Tumor immune microenvironment characterization in clear cell renal cell carcinoma identifies prognostic and immunotherapeutically relevant messenger RNA signatures.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
1. To identify potential effectors responsible for anti-tumorigenesis by targeting PLD1, we performed microarray in two Wnt-relevant colon cancer cells and analyzed transcriptional profile of genes that were differently expressed by inhibition and knockdown of PLD1
Publication Title
Targeting phospholipase D1 attenuates intestinal tumorigenesis by controlling β-catenin signaling in cancer-initiating cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 29 Downloadable Samples
- Illumina HiSeq 2000
Description
Memory stabilization after learning requires transcriptional and translational regulations in the brain, yet the temporal molecular changes following learning have not been explored at the genomic scale. We here employed ribosome profiling and RNA sequencing to quantify the translational status and transcript levels in mouse hippocampus following contextual fear conditioning. We identified 104 genes that are dynamically regulated. Intriguingly, our analysis revealed novel repressive regulations in the hippocampus: translational suppression of ribosomal protein-coding genes at basal state; learning-induced early translational repression of specific genes; and late persistent suppression of a subset of genes via inhibition of ESR1/ERa signaling. Further behavioral analyses revealed that Nrsn1, one of the newly identified genes undergoing rapid translational repression, can act as a memory suppressor gene. This study unveils the yet unappreciated importance of gene repression mechanisms in memory formation. Overall design: The application of ribosome profiling and RNA-seq techniques to mouse hippocampi tissues after contextual fear conditioning and to mouse hippocampal primary cultures. Mouse ESCs were also examined.
Publication Title
Multiple repressive mechanisms in the hippocampus during memory formation.
Sample Metadata Fields
No sample metadata fields
View Samples