Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from CSC and Non-CSC of three HCC cell lines

ABSTRACT: Hepatocellular carcinoma (HCC) represents the major subtype of liver cancer, characterized with a high rate of recurrence and heterogeneity. Liver cancer stem cells (CSCs) may account for a hierarchical organization of heterogeneous cancer cells. However, how liver CSCs sustain their self-renewal remains largely unknown. We used microarrays to discover the long non-coding RNAs (lncRNAs) expression underlying cell stem cell (CSC) and non cell stem cell (non-CSC) and identified distinct lncRNAs during this process. We sorted CD13+CD133+ and CD13-CD133- cells from Hep3B, Huh7, and PLC/PRF/5 HCC cell lines as liver CSCs and non-CSCs, then hybridized on Affymetrix microarrays. We sought to identify distinct lncRNAs in liver CSCs.

ORGANISM(S): Homo sapiens

SUBMITTER: Yanying Wang

PROVIDER: E-GEOD-66529 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data from CSC and Non-CSC of three HCC cell lines

Project description:Hepatocellular carcinoma (HCC) represents the major subtype of liver cancer, characterized with a high rate of recurrence and heterogeneity. Liver cancer stem cells (CSCs) may account for a hierarchical organization of heterogeneous cancer cells. However, how liver CSCs sustain their self-renewal remains largely unknown. We used microarrays to discover the long non-coding RNAs (lncRNAs) expression underlying cell stem cell (CSC) and non cell stem cell (non-CSC) and identified distinct lncRNAs during this process.

2015-03-05 | GSE66529 | GEO

Expression data from CSC and Non-CSC of three primary HCC samples

2019-07-10 | GSE122420 | GEO

snoRNA-sequencing analysis of liver cancer stem cells from human samples

Project description:To explore the role of small nucleolar RNA (snoRNA) on self-renewal of liver cancer stem cells (CSCs), we isolated liver CSCs (CD133+CD13+) and Non-CSCs (CD133-CD13-) from huamn liver tumor tissues.

2023-06-30 | GSE233521 | GEO

Expression data comparing CD133+ and CD133- B16-F10 melanoma cells

Project description:Cancer stem cells (CSC) were isolated based on the putative stem cell marker CD133. This subset of cells has been shown to have superior tumorigenicity and metastatic ability compared to cells in the non-CSC compartment (i.e. CD133-). We compared microRNA expression profiles of CSCs to non-CSCs to identify disparities in miRNA expression and explore how these miRNAs may provide a selective survival advantage to cancer stem cells.

2019-05-03 | GSE130283 | GEO

Expression data from CSC and Non-CSC of three primary HCC samples

Project description:Expression data from CSC and Non-CSC of three primary HCC samples

| PRJNA505166 | ENA

Expression data from human glioma cancer stem cell (CSC) specimens following knockdown of GREM1

Project description:CSCs differentially secrete the BMP antagonist Gremlin1 compared to non-stem glioma populations. Knockdown of Gremlin1 decreases CSC proliferation and tumorigenicity, establishing Gremlin1 as an essential effector for CSC maintenance. We used a microarray to determine the gene expression programs that are activated downstream of Gremlin1 that might be responsible for CSC maintenance. Glioma CSC cultures from two distinct patient-derived specimens (528 and 3691) were transduced with lentivirus expressing non-targeting scrambled shRNA or one of two distinct Gremlin1 shRNAs (shGrem1_485 and shGrem1_2456) for 72 hours (total of six samples). RNA was extracted for array hybridization.

2014-06-03 | E-GEOD-52846 | biostudies-arrayexpress

Expression data from human glioma cancer stem cell (CSC) specimens following knockdown of GREM1

2014-06-03 | GSE52846 | GEO

Genome-wide analysis of gene expression by IFNβ in Transformed HMEC (Epithelial/non-CSC, Mesenchymal/CSC)

Project description:Triple Negative Breast Cancer (TNBC), the deadliest form of this disease, lacks a targeted therapy. TNBC tumors that fail to respond to chemotherapy are characterized by a repressed Interferon/Signal Transducer and Activator of Transcription (IFN/STAT) gene signature and are often enriched for Cancer Stem Cells (CSCs). We have found that human mammary epithelial cells that undergo an Epithelial-to-Mesenchymal Transition (EMT) following transformation acquire CSC properties. These mesenchymal/CSCs have a significantly repressed IFN/STAT gene expression signature and an enhanced ability to migrate and form tumor spheres. Treatment with Interferon-Beta (IFNb) led to a less aggressive epithelial/non-CSC-like state, with repressed expression of mesenchymal proteins (VIMENTIN, SLUG), reduced migration and tumor sphere formation, and re-expression of CD24 (a surface marker for non-CSCs), concomitant with an epithelial-like morphology. The CSC-like properties were correlated with high levels of unphosphorylated Interferon Stimulated Gene Factor 3 (U-ISGF3), which was previously linked to resistance to DNA damage. Inhibiting the expression of IRF9 (the DNA-binding component of U-ISGF3) reduced the migration of mesenchymal/CSCs. Here we report a positive translational role for IFNb as gene expression profiling of patient derived TNBC tumors demonstrates that an IFNb Metagene signature correlates with improved patient survival, an immune response linked with Tumor Infiltrating Lymphocytes (TILs) and a repressed CSC Metagene signature. Taken together, our findings indicate that repressed IFN signaling in TNBCs with CSC-like properties is due to high levels of U-ISGF3, and that treatment with IFNb reduces CSC properties, suggesting a novel therapeutic strategy to treat drug-resistant, highly aggressive TNBC tumors.

2017-11-12 | GSE106782 | GEO

Gene expression profiles of pancreatic ductal adenocarcinoma cell lines differently co-expressing cancer stem cell markers

Project description:Pancreatic cancer stem cells (CSCs) have been described as CD24+/CD44+/EpCAM+ or CD133+ cells. However, no study has determined the co-expression of all of these markers in pancreatic ductal adenocarcinoma. Similarly to other combinations of CSC markers, CD24+/ CD44+/EpCAM+/CD133+ phenotype might more accurately identify true pancreatic CSCs. Therefore, we performed a detailed co-expression analysis of CD24, CD44, EpCAM, and CD133 in 3 cell lines derived from primary pancreatic ductal adenocarcinomas (PDACs). Gene expression profiling was applied in order to further investigate the observed differences in proportion of cells that co-expressed CSC markers among the cell lines.

2016-02-29 | E-MTAB-4055 | biostudies-arrayexpress

Curcumin Effectively Depletes Hepatic Cancer Stem-Like Cells

Project description:The cancer stem cells (CSCs) have important therapeutic implications for multi-resistant cancers including hepatocellular carcinoma (HCC). Among the key pathways frequently activated in liver CSCs is NF-kB signaling. Here we evaluated the CSCs-depleting potential of NF-kB inhibition in liver cancer achieved by IKK inhibitor curcumin and specific peptide SN50 . The effects on CSCs were assessed by analysis of Side Population (SP) and expression levels of CSC-related genes as determined by RT-qPCR, gene expression microarray, EMSA, and Western blotting. Curcumin caused anti-proliferative and pro-apoptotic responses directly related to the extent of NF-kB inhibition. In curcumin-sensitive tumor cells, the treatment led to a selective CSC depletion as evidenced by a reduced SP size, decreased sphere formation, down-regulation of CSC markers and suppressed tumorigenicity. Similarly, NF-kB inhibition by SN50 caused a general suppression of cell growth accompanied by a reduced SP fraction. In contrast, curcumin-resistant cells exhibited a paradoxical increase in proliferation and expression of CSC markers. Mechanistically, CSC-depleting activity of curcumin was exerted by the NF-kB-mediated HDAC inhibition causing down-regulation of c-MYC and other key oncogenic targets. Co-administration of the class I/II HDAC inhibitor trichostatine sensitized resistant cells to curcumin. Further, integration of a predictive signature of curcumin sensitity with our HCC database indicated that HCC patients with poor prognosis and progenitor features are most likely to benefit from NF-kB inhibition. These results demonstrate that NF-kB inhibition can specifically target CSC populations and suggest a potential for combined inhibition of NF-kB and HDAC signaling for treatment of liver cancer patients with poor prognosis. Five human hepatoma cell lines with and without curcumin

2015-12-31 | E-GEOD-59713 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data