Synthetic construct
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA362884 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Oncogenic activation of RNA binding proteins and c-Myc signaling in hepatocellular carcinoma
| PRJNA296391 | ENA
Project description:Global transcriptomic alterations of both coding and non-coding RNA species are a ubiquitous feature associated with human cancers including hepatocellular carcinoma (HCC). Dysregulation of RNA-binding proteins (RBPs), the key regulators of RNA processing, is one mechanism in which cancer cells select to promote tumorigenesis. We analyzed genomic alterations amongst a family of more than 800 mRNA RBPs (mRBPs) in 1,225 clinical specimens from HCC patients and found that RBPs are significantly activated through gene amplification in a subset of tumors with poor prognosis, suggesting their potential oncogenic roles in HCC progression. Amongst the top candidates, RD binding protein (RDBP) was further characterized for its oncogenic role and effects on the HCC transcriptome. While the activation of RDBP induced an oncogenic phenotype, the abrogation of RDBP in HCC cells significantly decreased cancer associated phenotypes such as cell proliferation, migration/invasion and tumorigenicity in vivo. Further microarray analyses revealed that RDBP-dependent genes were tumor-related with a significant enrichment for c-Myc targets, suggesting interplay between RDBP and c-Myc signaling. Similar data were also found in HCC clinical specimens where c-Myc amplification was uncommon. Consistently, the RDBP-dependent c-Myc target gene signature was able to predict HCC patient survival in two independent cohorts of more than 400 patients. Taken together, our results suggest that oncogenic activation of RDBP is a novel mechanism that contributes to global transcriptome imbalance that is selective for the activation of c-Myc oncogenic signaling in HCC. We used microarray analysis to determine the affects of siRNA mediated RDBP knockdown in HCC transcriptome in cell lines. Hep3b and Huh1 cells were transfected with RDBP or scramble control siRNA for 48 hours in quadruplicates. Quality control using Spearman or Pearson correlation removes outliers resulting in triplicates for each group
2015-09-23 | E-GEOD-73219 | biostudies-arrayexpress
Project description:<p>Hepatocellular carcinoma (HCC) is a highly aggressive form of carcinoma with a poor prognosis. Diagnostic markers and potential therapeutic targets for HCC are urgently needed. Here, we demonstrate that fecal microbiota transplantation (FMT) using stool samples from HCC patients significantly promote the growth of patient-derived xenografts (PDXs). 16s-rRNA sequencing combined with qPCR reveal that Streptococcus anginosus (S. anginosus) is enriched in the stool samples of HCC patients and HCC-FMT mice. S. anginosus monocolonization recapitulates the tumor-promoting effect of HCC-FMT in germ-free (GF) mice. Mechanistically, S. anginosus plays a critical role in regulating the downstream pathways of BRD4 via its metabolites, thereby promoting the activation of oncogenic Myc and E2F signaling pathways, HCC progression and BET inhibitor (BETi) resistance. S. anginosus-derived lactate promotes BRD4 lactylation at the K317 site via AARS1, thereby inhibiting BRD4 ubiquitination and degradation. Notably, blockade of the S. anginosus-BRD4 lactylation axis improves the BETi responsiveness in both syngeneic mouse models and PDXs. Overall, our study highlights the oncogenic role of the S. anginosus-BRD4 signaling in the gut-liver axis and suggests its potential as a non-invasive biomarker and therapeutic target for HCC.</p>
2025-12-05 | MTBLS12398 | MetaboLights
Project description:Differences in DNA-binding specificity of floral homeotic protein complexes predict organ-specific target genes
| PRJNA378233 | ENA
Project description:Global transcriptomic alterations of both coding and non-coding RNA species are a ubiquitous feature associated with human cancers including hepatocellular carcinoma (HCC). Dysregulation of RNA-binding proteins (RBPs), the key regulators of RNA processing, is one mechanism in which cancer cells select to promote tumorigenesis. We analyzed genomic alterations amongst a family of more than 800 mRNA RBPs (mRBPs) in 1,225 clinical specimens from HCC patients and found that RBPs are significantly activated through gene amplification in a subset of tumors with poor prognosis, suggesting their potential oncogenic roles in HCC progression. Amongst the top candidates, RD binding protein (RDBP) was further characterized for its oncogenic role and effects on the HCC transcriptome. While the activation of RDBP induced an oncogenic phenotype, the abrogation of RDBP in HCC cells significantly decreased cancer associated phenotypes such as cell proliferation, migration/invasion and tumorigenicity in vivo. Further microarray analyses revealed that RDBP-dependent genes were tumor-related with a significant enrichment for c-Myc targets, suggesting interplay between RDBP and c-Myc signaling. Similar data were also found in HCC clinical specimens where c-Myc amplification was uncommon. Consistently, the RDBP-dependent c-Myc target gene signature was able to predict HCC patient survival in two independent cohorts of more than 400 patients. Taken together, our results suggest that oncogenic activation of RDBP is a novel mechanism that contributes to global transcriptome imbalance that is selective for the activation of c-Myc oncogenic signaling in HCC. We used microarray analysis to determine the affects of siRNA mediated RDBP knockdown in HCC transcriptome in cell lines.
2015-09-23 | GSE73219 | GEO
Project description:Unraveling determinants of transcription factor binding outside the core binding site
| PRJNA275965 | ENA
Project description:Differential binding cell-SELEX development
| PRJNA475197 | ENA
Project description:genotypes of fluorescent protein variants
| PRJNA540481 | ENA
Project description:Single fluorescent protein biosensor engineering
| PRJNA324720 | ENA
Project description:genotypes of fluorescent protein variants
| PRJNA631354 | ENA