Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Current androgen deprivation induces androgen receptor-independent prostate cancer via HGF and Wnt activation to foster nuclear export and ribosome biogenesis [RNA-seq]

ABSTRACT: Current androgen deprivation induces androgen receptor-independent prostate cancer via HGF and Wnt activation to foster nuclear export and ribosome biogenesis [RNA-seq]

PROVIDER: PRJNA940660 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23693774_1.fastq.gz	Fastqsanger.gz
	SRR23693774_2.fastq.gz	Fastqsanger.gz
	SRR23693775_1.fastq.gz	Fastqsanger.gz
	SRR23693775_2.fastq.gz	Fastqsanger.gz
	SRR23693776_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

Current androgen deprivation induces androgen receptor-independent prostate cancer via HGF and Wnt activation to foster nuclear export and ribosome biogenesis [scRNA-Seq]

Project description:Current androgen deprivation induces androgen receptor-independent prostate cancer via HGF and Wnt activation to foster nuclear export and ribosome biogenesis [scRNA-Seq]

| PRJNA940676 | ENA

Current androgen deprivation induces androgen receptor-independent prostate cancer via HGF and Wnt activation to foster nuclear export and ribosome biogenesis [scRNA-Seq]

Project description:To inhibit the re-activation of AR-promoted tumor growth via residual androgens, more potent AR antagonists and inhibitors for androgen synthesis have been developed in the decades. While these second-generation antagonists/inhibitors showed some effectiveness clinically, they also induced more diverse CRPC phenotypes. Specifically, a subpopulation of AR- and neuroendocrine (NE)-null PC cells, DNPC, occurs frequently in CRPC patients treated with abiraterone and enzalutamide, increasing metastatic CRPC incidences and the mortality of PCa. Understanding the mechanisms for DNPC will directly improve clinical outcomes.

2023-12-21 | GSE226555 | GEO

Current androgen deprivation induces androgen receptor-independent prostate cancer via HGF and Wnt activation to foster nuclear export and ribosome biogenesis [RNA-seq]

Project description:To inhibit the re-activation of AR-promoted tumor growth via residual androgens, more potent AR antagonists and inhibitors for androgen synthesis have been developed in the decades. While these second-generation antagonists/inhibitors showed some effectiveness clinically, they also induced more diverse castration-resistant prostate cancer (CRPC) phenotypes. Specifically, a subpopulation of AR- and neuroendocrine (NE)-null PC cells, DNPC, occurs frequently in CRPC patients treated with abiraterone and enzalutamide, increasing metastatic CRPC incidences and the mortality of prostate adenocarcinoma (PCa). Understanding the mechanisms for DNPC will directly improve clinical outcomes.

2023-12-21 | GSE226547 | GEO

Androgen deprivation induces double-null prostate cancer via aberrant activation of nuclear export and ribosomal biogenesis by HGF and Wnt axes

Project description:Androgen deprivation induces double-null prostate cancer via aberrant activation of nuclear export and ribosomal biogenesis by HGF and Wnt axes

| PRJNA940671 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of HGF treated (HGF+) and matched control (HGF-) HepG2 cells

Project description:We report the high-throughput profiling of HGF treated liver cancer cell (HepG2) for differentiated genes analysis. We generated HGF stimulated and paired control HepG2 cells for 4 days. We find that tumor suppressor genes that are overexpressed and some tumor associated genes were downregulated, therefore reflect cell state and HGF induced anti-tumor potential. This study provides a potential framework for the research of HGF induced critical genes in the application of liver cancer therapy.

2021-12-30 | GSE133424 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of HGF treated (HGF+) and matched control (HGF-) HepG2 cells

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of HGF treated (HGF+) and matched control (HGF-) HepG2 cells

| PRJNA551437 | ENA

HepG2 Cell: Control vs. HGF treated

Project description:Transcription profile of HepG2 cells treated with hepatocyte growth factor and control cells Two condition experiment, Hep G2 vs. Hep G2-HGF. Biological replicates: 1 control and 1 HGF-treated (no replication)

2012-02-23 | E-GEOD-35994 | biostudies-arrayexpress

Expression array analysis of the hepatocyte growth factor (HGF) invasive program

Project description:HGF stimulates mitogenesis, motogenesis and morphogenesis in most epithelial target cells. Selective inhibition of HGF signaling blocks spontaneous metastasis, but not primary tumor growth, in the prostate adenocarcinoma derived PC3M cell xenograft model. To identify the HGF activated genes and pathways that contribute to cell motility and invasion, i.e. the HGF invasive program, expression profiling was performed on PC3M cells that were untreated or were treated with human HGF (hHGF), which drives all 3 primary activities, or with human HGF/NK2 (hNK2) or murine HGF (mHGF), which drive motility and invasion but not proliferation in human cells. Differences in gene expression profiles among these four groups were used to distiniguish between events associated with invasion (resulting from hNK2 or mHGF treatment) from those associated with the combination of invasion and proliferation (resulting from hHGF treatment).

2015-08-25 | GSE71404 | GEO

Functional Comparison of the HGF/Met and MSP/Ron Systems in a Pancreatic Cancer Model

Project description:Pancreatic cancer is an aggressive disease with a poor prognosis for which current standard chemotherapeutic treatment options offer little survival benefit. In recent years, receptor tyrosine kinases (RTK)s have garnered interest as therapeutic targets to augment or replace standard chemotherapeutic therapies because of their high expression levels in various cancers and their ability to promote cell growth, migration, and survival. Met and Ron, which are homologous RTKs activated by the ligands hepatocyte growth factor (HGF) and macrophage stimulating protein (MSP), respectively, are over-activated in many of the least treatable cancers. In pancreatic adenocarcinoma, Met expression is linked to poor patient survival and Ron expression is generally higher in tumor samples relative to normal tissue, although its prognostic significance in pancreatic cancer remains unclear. Despite the structural homology between Met and Ron, studies that have directly compared the functional outcomes of these systems in any context are limited. To address this, we sought to determine if the HGF/Met and MSP/Ron systems produce overlapping or divergent contributions towards a malignant phenotype by performing a characterization of MSP and HGF driven signaling, behavioral, and transcriptomic responses in pancreatic cancer cells in vitro. We found HGF and MSP both encouraged cell migration and activated the MAPK/Erk pathway both at the transcript and protein level. HGF uniquely increased proliferation in addition to regulating a wider variety of transcripts compared to MSP. Although HGF and MSP produced a differing breadth of responses, overlapping pro-cancer signaling, behavioral, and transcriptional effects suggest dual inhibition of the MSP/Ron and HGF/Met systems in pancreatic cancer may provide a more complete anti-cancer effect compared to individually targeting either system.

2019-06-14 | GSE129075 | GEO

Transcriptomic and Proteomic Response of HC-04 to hepatocyte growth factor (HGF)

Project description:The routine study of human malaria liver-stage biology in vitro is hampered by low infection efficiency of human hepatocellular carcinoma (HCC) lines (<0.1%), poor understanding of steady-state HCC biology, and lack of appropriate tools for trace sample analysis. HC-04 is the only HCC that supports complete development of human malaria parasites. We hypothesized that HCCs are in various intermediate stages of the epithelial-mesenchymal transition (EMT) and HC-04s retain epithelial characteristics that permit infection. We developed an novel analytical approach to test this hypothesis viz. the HC-04 response to hepatocyte growth factor (HGF). We used online two-dimensional liquid chromatography tandem mass spectrometry (2D-LC-MS/MS) to quantify protein expression profiles in HC-04 pre-/post-HGF treatment and validated these results by RT-qPCR and microscopy. We successfully increased protein identification efficiency over offline-2D methods by 12-fold using less sample material, allowing robust protein quantification. We observed expected up-regulation and down-regulation of EMT protein markers in response to HGF, but also unexpected cellular responses. HC-04 is thus susceptible to HGF-mediated signaling but to a lesser degree than what we observed for HepG2, a widely used, but poor malaria HCC model. Our analytical approach to understanding the basic biology of HC-04 helps us understand the factors that may influence its utility as a model for malaria liver-stage development. We observed that HC-04 treatment with HGF prior to the addition of Plasmodium falciparum sporozoites did not facilitate cell invasion, arguing for unlinking the effect of HGF on malaria liver stage development from hepatocyte invasion. Finally, our 2D-LC-MS/MS approach and broadly applicable experimental strategy should prove useful in the analysis of various hepatocyte-pathogen interactions, tumor progression and early disease events.

2014-02-17 | PXD000682 | Pride

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