Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CCDC137 in HCC cells

ABSTRACT: CCDC137 in HCC cells

PROVIDER: PRJNA902306 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22273651_1.fastq.gz	Fastqsanger.gz
	SRR22273651_2.fastq.gz	Fastqsanger.gz
	SRR22273652_1.fastq.gz	Fastqsanger.gz
	SRR22273652_2.fastq.gz	Fastqsanger.gz
	SRR22273653_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Human HCC cells

Project description:Human HCC cells Raw sequence reads

| PRJNA884272 | ENA

GNPS_Steatohepatitis progresses to cancer via immunosuppression of HCC directed CD8+ T cells

Project description:Steatohepatitis progresses to cancer via immunosuppression of HCC directed CD8+ T cells LC/MS data of intestinal content in murine model. Multiple categories associated with normal and high fat diet, NAFLD, NASH and HCC are included.

2017-04-13 | MSV000080918 | GNPS

The gene expression of HCC cells and HCC cells knocked down TMED3

Project description:We report that TMED3 was up-regulated in HCC and portal vein tumor thrombus. Gene microarray analysis TMED3-knockdown cells and normal HCC cell.

2017-02-09 | GSE88772 | GEO

Genes regulated by SMAD3 in HCC cells

Project description:Genes regulated by SMAD3 in HCC cells

| PRJNA548278 | ENA

Inhibition of YAP in human HCC cells

Project description:Inhibition of YAP in human HCC cells

| PRJNA498280 | ENA

FIR inhibition in HCC cells (Hep3B)

Project description:siRNA-mediated inhibition compared to untreated cells and cells transfected with nonsense siRNA Together with far upstream element binding protein (FBP), the FBP-interacting repressor (FIR) represents a molecular tool for the transcriptional fine tune regulation of target genes. Previous evidence indicates that strong overexpression of FBP in human hepatocellular carcinoma (HCC) supports tumor growth and correlates with poor patient prognosis. However, the role of the transcriptional repressor FIR in hepatocarcinogenesis remains poorly delineated. We show that overexpression of FIR correlates with tumor dedifferentiation and tumor cell proliferation in about 60% of primary HCCs. Elevated FIR levels are associated with genomic gains of the fir gene locus at chromosome 8q24.3 in human HCC specimens. In vitro, nuclear enrichment of FIR supports HCC cell proliferation and migration. Expression profiling of HCC cells after siRNA-mediated silencing of FIR identified the transcription factor DP-1 (TFDP1) as a transcriptional target of FIR. Surprisingly, FIR stimulates the expression of FBP in a TFDP1/E2F-dependent manner. FIR splice variants lacking or containing exon 2 and/or exon 5 are expressed in the majority of HCCs. Specific inhibition of FIR isoforms with and without exon 2 revealed that all FIR splice variants facilitate tumor-supporting effects. This finding was confirmed in xenograft transplantation experiments with lentiviral-infected shRNA targeting all FIR variants as well as FIR with and without exon 2. In summary, high-level nuclear FIR does not facilitate repressor properties but supports tumor growth in HCC cells. Thus, the pharmacological inhibition of FIR might represent a promising therapeutic strategy for HCC patients. Expression profiling of cells transfected with scrambled/nonsense siRNA (control), and after siRNA-mediated FIR inhibition.

2014-09-03 | E-GEOD-55692 | biostudies-arrayexpress

YAP Inhibition in HCC cells (Hep3B)

Project description:siRNA-mediated inhibition compared to untreated cells and cells transfected with nonsense siRNA. Loss of contact inhibition and anchorage-independent growth are hallmarks of cancer cells. In this context, frequent inactivation of the Hippo pathway and subsequent nuclear enrichment of the transcriptional coactivator yes-associated protein (YAP) uncouple cell proliferation and anti-apoptosis from contact inhibition, associated with uncontrolled tumor growth and tumor cell dissemination. However, general molecular mechanisms of tumor-supporting YAP activity remain unclear. In this study, we show that overexpression and nuclear accumulation of YAP in hepatocytes and hepatocellular carcinoma (HCC) cells leads to an induction of the Notch pathways through transcriptional activation of the Notch ligand jagged-1 (Jag-1). This induction of Jag-1 strictly depends on binding of YAP to TEAD4 and does not rely on WNT/β-catenin pathway activity. Co-activation of YAP, TEAD4, Jag-1, and the Notch target gene Hes-1 was significantly higher in HCC from patients with poor prognosis. High-level expression and nuclear accumulation of YAP correlates with Jag-1/Notch activation not only in human HCC tissues, but also in colon and pancreatic cancer tissues. Thus, our data demonstrate that YAP-driven co-activation of the Jag-1/Notch pathway in part facilitates oncogenic properties of the oncogene YAP not only in HCC but also in different gastrointestinal malignancies. Expression profiling of untreated HCC cell lines (control 1), cells transfected with scrambled/nonsense siRNA (control 2), and after siRNA-mediated YAP inhibition.

2012-11-01 | E-GEOD-35004 | biostudies-arrayexpress

Expression data from SOX9 knockdown in HCC cells

Project description:Expression data from SOX9 knockdown in HCC cells

| PRJNA600736 | ENA

Expression data from TGFβ1(TGFbeta1) treated HCC cells

Project description:Expression data from TGFβ1(TGFbeta1) treated HCC cells

| PRJNA809387 | ENA

Transcriptome alteration upon ZNF281 depletion in HCC cells

Project description:Transcriptome alteration upon ZNF281 depletion in HCC cells

| PRJNA610754 | ENA