Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257733 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We identified a novel mechanism by which IL-6/STAT3 signaling up-regulates CD133 expression and promotes HCC progression. STAT3 activation upregulates the expression of CD133 during liver carcinogenesis. Targeting STAT3-mediated CD133 overexpression may represent a promising therapeutic strategy for HCC patients via eradicating the liver tumor microenviornment. To develop novel cancer therapeutic strategies by identification of signaling pathways or biomarkers and understanding their functions on cancer stem cell biology, we determined CD133 expression and STAT3 activation with tumor microenvironment in HCC patient tissues. The relation of STAT3 activation and CD133 expression was investigated by luciferase assay, shRNA knock-down, and chromatin immunoprecipitation assay in HCC cells, and in vivo xenograft model.
2014-08-08 | E-GEOD-60194 | biostudies-arrayexpress
Project description:We identified a novel mechanism by which IL-6/STAT3 signaling up-regulates CD133 expression and promotes HCC progression. STAT3 activation upregulates the expression of CD133 during liver carcinogenesis. Targeting STAT3-mediated CD133 overexpression may represent a promising therapeutic strategy for HCC patients via eradicating the liver tumor microenviornment.
2014-08-08 | GSE60194 | GEO
Project description:To demonstrate CD133+CD44+ and CD133+CD44- subpopulations of hepatocellular carcinoma as distinct subgroups, we have employed whole genome microarray expression profiling as a discovery platform to reveal the gene profiles of different subgroups and identify genes responsible for the enhanced metastatic potentials of CD133+CD44+ tumor cells. CD133+CD44+ and CD133+CD44- tumor cells were isolated from three human metastatic hepatocellular carcinoma specimens. A 76-gene consensus signature was identified that distinguished between CD133+CD44+ and CD133+CD44- subgroups. CD133+CD44+ and CD133+CD44- subgroups from different patients were well clustered as two distinct classes according to this signature, and many genes in this signature were reported involved in tumor metastasis. Expression of four genes (CCL4, DKK3, CCR5 and MMP12) from this signature was confirmed in another three metastatic HCC specimens by real-time PCR. CD133+CD44+ and CD133+CD44- subpopulations of hepatocellular carcinoma were isolated from three metastatic hepatocellular carcinoma specimens by flow cytometry. A total of 30K to 50K cells for each subgroup was obtained for each microarray.
2010-12-28 | E-GEOD-26321 | biostudies-arrayexpress
Project description:CCN3 is a therapeutic target that promotes OPN upregulation and coagulation cascades activation in hepatocellular carcinoma
| PRJNA360277 | ENA
Project description:To demonstrate CD133+CD44+ and CD133+CD44- subpopulations of hepatocellular carcinoma as distinct subgroups, we have employed whole genome microarray expression profiling as a discovery platform to reveal the gene profiles of different subgroups and identify genes responsible for the enhanced metastatic potentials of CD133+CD44+ tumor cells. CD133+CD44+ and CD133+CD44- tumor cells were isolated from three human metastatic hepatocellular carcinoma specimens. A 76-gene consensus signature was identified that distinguished between CD133+CD44+ and CD133+CD44- subgroups. CD133+CD44+ and CD133+CD44- subgroups from different patients were well clustered as two distinct classes according to this signature, and many genes in this signature were reported involved in tumor metastasis. Expression of four genes (CCL4, DKK3, CCR5 and MMP12) from this signature was confirmed in another three metastatic HCC specimens by real-time PCR.
2010-12-28 | GSE26321 | GEO
Project description:p-STAT3 has emerged as a critical modulator of hepatocellular carcinoma (HCC) progression; however, its role in 3D chromatin architecture and the expression of genes linked to HCC aggressiveness remains largely unexplored. Here, we elucidate the function of p-STAT3 in establishing stable regulatory regions known as FIREs, characterized by highly active interactions and the potential to alter topologically associated domains (TADs). Our results demonstrate that expression of genes located within FIREs is highly correlated, and upregulation, these genes play a crucial role in driving phenotypes, including HCC invasion and tube formation. Notably, p-STAT3-associated FIREs maintain chromatin activation despite pharmacological interventions targeting STAT3, suggesting a mechanism that failure to suppress the expression of genes associated with HCC aggressiveness leads to drug resistance. These findings provide novel insights into how the 3D genome structure associated with p-STAT3 promotes HCC progression and drug resistance, highlighting the therapeutic potential of targeting 3D chromatin dynamics in HCC.
2025-11-26 | GSE275343 | GEO
Project description: Not available
| S-EPMC2531291 | biostudies-literature