Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The NALCN channel regulates metastasis and non-malignant cell dissemination (Bulk RNA-Seq)

ABSTRACT: The NALCN channel regulates metastasis and non-malignant cell dissemination (Bulk RNA-Seq)

PROVIDER: PRJNA863886 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR20721700_1.fastq.gz	Fastqsanger.gz
	SRR20721700_2.fastq.gz	Fastqsanger.gz
	SRR20721701_1.fastq.gz	Fastqsanger.gz
	SRR20721701_2.fastq.gz	Fastqsanger.gz
	SRR20721702_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 206

Similar Datasets

The NALCN channel regulates metastasis and non-malignant cell dissemination

Project description:The NALCN channel regulates metastasis and non-malignant cell dissemination

| PRJNA863884 | ENA

The NALCN channel regulates metastasis and non-malignant cell dissemination (Bulk RNA-Seq)

Project description:We identify the Sodium Leak Channel Non-Selective Protein (NALCN) as a key regulator of cancer metastasis and non-malignant cell dissemination. Among 10,022 human cancers, NALCN loss-of-function mutations were enriched in gastric and colorectal cancers. Deletion of Nalcn from gastric, intestinal or pancreatic adenocarcinomas in mice did not alter tumour incidence, but markedly increased the number of circulating tumour cells (CTCs) and metastases. Treatment of these mice with gadolinium–a NALCN channel blocker–similarly increased CTCs and metastases. Deletion of Nalcn from mice that lacked oncogenic mutations and never developed cancer, caused shedding of epithelial cells into the blood at levels equivalent to those seen in tumour-bearing animals. These cells trafficked to distant organs to form normal structures including lung epithelium and kidney glomeruli and tubules. Thus, NALCN regulates cell shedding from solid tissues independent of cancer, divorcing this process from tumourigenesis and unmasking a potential new target for anti-metastatic therapies.

2022-08-06 | GSE210133 | GEO

The NALCN channel regulates metastasis and non-malignant cell dissemination (scRNA-Seq)

Project description:The NALCN channel regulates metastasis and non-malignant cell dissemination (scRNA-Seq)

| PRJNA863885 | ENA

The NALCN channel regulates metastasis and non-malignant cell dissemination (scRNA-Seq)

2022-08-06 | GSE210132 | GEO

Non-programmed dissemination of cancer cell clusters induce malignant properties through Integrin beta 1 activation

Project description:We found that epithelial cluster recruiment soluble fibronectin and then activating beta1 Integrin induce epithelial-mesenchymal transition and enhance cancer cells’ malignant after cell dissemination. Non-programmed dissemination of cluster cells triggers ERK cascade and then accelerate tumor growth and metastasis. Our finding reveals that cell cluster plays a vital role in the non-programmed dissemination of breast cancer cells’ metastasis, offering a potential new therapeutic target for metastasis patients.

2022-12-31 | GSE173538 | GEO

PHGDH heterogeneity potentiates cancer cell dissemination and metastasis

Project description:Cancer metastasis requires the transient activation of cellular programs enabling dissemination and seeding in distant organs. Genetic, transcriptional and translational heterogeneity contributes to this dynamic process. Metabolic heterogeneity has also been observed, yet its role for cancer progression is less explored. Here, we discover that loss of phosphoglycerate dehydrogenase (PHGDH) potentiates metastatic dissemination. Specifically, we find that heterogeneous or low PHGDH expression in primary tumors of breast cancer patients is associated with decreased metastasis free survival time. In mice, circulating tumor cells and early metastatic lesions are enriched with PHGDH low cancer cells and silencing PHGDH in primary tumors increases metastasis formation. Mechanistically, PHGDH protein interacts with the glycolytic enzyme phosphofructokinase (PFK) and the loss of this interaction activates the hexosamine – sialic acid pathway, which provides precursors for protein glycosylation. Consequently, aberrant protein glycosylation including increased sialylation of integrin αvβ3 occurs, which potentiates cell migration and invasion. Inhibition of sialic acid metabolism counteracts the metastatic capacity of PHGDH low cancer cells. In conclusion, while the catalytic activity of PHGDH supports cancer cell proliferation, low PHGDH protein expression non-catalytically potentiates cancer dissemination and metastasis formation. Thus, the presence of PHDGH heterogeneity in primary tumors may be considered a sign of tumor aggressiveness.

2022-03-30 | GSE198380 | GEO

The NALCN channel regulates metastasis and non-malignant cell dissemination

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-06 | GSE210134 | GEO

PHGDH heterogeneity potentiates cancer cell dissemination and metastasis

Project description:PHGDH heterogeneity potentiates cancer cell dissemination and metastasis

| PRJNA814732 | ENA

Malignant ascites microenvironment induced macrophage reprogramming facilities epithelial ovarian cancer peritoneal metastasis

Project description:Macrophages form a primary immune cells population in tumor tissues and malignant ascites microenvironment (MAM). They can be activated and polarized into tumor-associated macrophages (TAM) by the embedded environment and promote tumor progression and metastasis However, the molecular mechanisms of MAM in macrophage polarization and the effects on epithelial ovarian cancer (EOC) metastatic progression remain elusive. Here, we found that that MAM modulates RhoA-GTPase-F-actin-Hippo signaling cascade in facilitating M2-like macrophage polarization that, in turn, promotes tumor dissemination. PUFA enriched magligant ascites microenvironment promote macrophage lipid oxidative phosphorylation and supression RhoA-GTPase-Yap1 axis. Genetic ablation Yap1 in macrophage exhibited M2-like polarization and enhanced ovrian tumor dissemination. Pharmacology inhibit Mst1/2 could rescue M2-like TAM polarization in MAM and alter the lipid oxidation of macrophages in MAM, more importantly, inhibit ovarian metastatic properties. Through comparasion primary TAM (P-TAM) and metastasis TAM (M-TAM), we proved that Hippo-Yap1 siganl results M-TAM with high M2/M1 ratio. These findings implicate critical functions of PUFA modulate RhoA-Hippo axis in facility TAM polarization and also suggest manipulation of PUFA metabolism or RhoA-Hippo siganl as a therapeutic strategy aganist EOC metastasis.

2024-05-01 | GSE175552 | GEO

ECM-dependent gene expression in normal and tumor-derived mammary organoids

Project description:A critical step in metastasis is cancer cell dissemination. Dissemination and metastasis are associated with specific genetic changes and changes in extracellular matrix (ECM), but how these changes interact to enable dissemination remains unclear. Here we tested the importance of ECM to dissemination in both normal and malignant mammary epithelium. By time-lapse imaging, we observed collective invasion and dissemination directly in 3D culture. Our results reveal that the pattern of epithelial migration and local dissemination are constrained by the local ECM microenvironment. To identify RNA expression changes that could regulate these changes in cell behavior, we conducted whole genome RNA expression profiling from normal and malignant mammary epithelium in 3D culture. We collected RNA from normal and malignant epithelium during active growth at 4 days in culture in either Matrigel or collagen I. We hybridized the resulting RNA to Agilent single color microarrays with a minimum of three biologically independent microarray replicates per condition. We observed significant gene expression differences between normal and malignant epithelium, even when cultured in the same ECM. In contrast, the ECM microenvironment had a relatively small impact on RNA expression, despite its large effects on migratory strategy and local dissemination. Gene expression was measured in normal and malignant mammary epithelial fragments cultured in one of two 3D matrices (laminin-rich basement membrane gel or collagen I) and collected at day 4, which we observed to have peak invasion and dissemination. At least three independent experiments were performed at each time using different mice for each experiment.

2012-08-16 | E-GEOD-39173 | 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