Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Knockdown of Ror2 in lineage-depleted tumor cells were derived from 2225L basal-like TP53 null mammary tumor models

ABSTRACT: We elucidated the function of the alternative Wnt receptor Ror2 in lineage-depleted tumor organoid cells, using lentiviral short hairpin RNA (shRNA)-mediated depletion.

ORGANISM(S): Mus musculus

PROVIDER: GSE174506 | GEO | 2022/10/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Knockdown of Ror2 in lineage-depleted tumor cells were derived from 2153L basal-like TP53null mammary tumor models

Project description:We elucidated the function of the alternative Wnt receptor Ror2 in lineage-depleted tumor organoid cells, using lentiviral short hairpin RNA (shRNA)-mediated depletion.

2022-10-26 | GSE176041 | GEO

Knockdown of Ror2 in lineage-depleted tumor cells were derived from 2225L basal-like TP53 null mammary tumor models

Project description:Knockdown of Ror2 in lineage-depleted tumor cells were derived from 2225L basal-like TP53 null mammary tumor models

| PRJNA730309 | ENA

Gene transcript alterations exhibited in luminal and basal epithelial compartments with impaired Ror2 signaling

Project description:Microarray analyses revealed distinct gene expression alterations in the luminal and basal epithelial compartments in the absence of Ror2 with marked alterations observed in genes associated with actin filament-based processes and the actin cytoskeletal network. Given that Ror2 expression resides in both basal and luminal epithelial cells, we wanted to identify compartment-specific functions for Ror2 in coordinating development. Accordingly, luminal and basal epithelial cell populations from shLUC and shRor2 outgrowths were isolated by FACS separation on the basis of CD24 and CD29 surface marker expression and gene expression analysis was subsequently performed using Agilent microarrays.

2015-01-09 | E-GEOD-57985 | biostudies-arrayexpress

Cell fate and adhesion dynamics rely on Ror2-mediated alternative Wnt signaling during tumor progression

Project description:Cellular heterogeneity in breast cancer encompasses many features, yet an understanding of the coexistence and regulation of various tumor cell subpopulations remains a significant challenge in cancer biology. In the current study, we approached tumor cell heterogeneity from the perspective of Wnt pathway biology to address how different modes of Wnt signaling shape the behaviors of diverse cell populations within a heterogeneous tumor landscape. Using a syngeneic TP53 null mouse model of breast cancer, we identified distinctions in the topology of canonical Wnt b-catenin dependent signaling activity and noncanonical b-catenin independent Ror2-mediated Wnt signaling across subtypes and within tumor cell subpopulations in vivo. We further discovered an antagonistic role for Ror2 in regulating canonical Wnt/b-catenin activity in vivo, where lentiviral shRNA depletion of Ror2 expression augmented canonical Wnt/b-catenin signaling activity across multiple basal-like models. Depletion of Ror2 expression yielded distinct phenotypic outcomes and divergent alterations in gene expression programs among different tumors, despite all sharing basal-like features. Notably, we uncovered cell state plasticity and adhesion dynamics regulated by Ror2, where Ras Homology Family Member A (RhoA) and Rho-Associated Coiled-Coil Kinase 1 (ROCK1) activity downstream of Dishevelled-2 (Dvl2) were implicated. Collectively, these studies illustrate the integration and collaboration of Wnt pathways in basal-like breast cancer, where Ror2 provides a spatiotemporal function to regulate the balance of Wnt signaling and cellular heterogeneity during tumor progression.

2017-01-23 | GSE93815 | GEO

WNT11/ROR2 signaling is associated with tumor invasion and poor survival in breast cancer

Project description:Breast cancer has been associated with activation of the WNT signaling pathway, although the underlying molecular mechanisms are still unclear. In order to understand the molecular basis of these observations, we overexpressed ROR2 in human breast cancer cell lines and characterized them by RNA-Sequencing. High levels of ROR2 were associated with defects in cell morphology and cell-cell-contacts leading to increased tumor invasiveness. Using gene expression analysis we demonstrated an upregulation of several non-canonical WNT ligands in ROR2-overexpressing breast cancer cells, in particular WNT11. Knockdown of WNT11 reversed the pro-invasive phenotype and the cellular changes in ROR2-overexpressing cells. Taken together, our studies revealed a novel auto-stimulatory loop in which ROR2 triggers the expression of its own ligands, e.g. WNT11, resulting in enhanced tumor invasion associated with breast cancer metastasis.

2022-02-21 | GSE161864 | GEO

Gene transcript alterations exhibited in luminal and basal epithelial compartments with impaired Ror2 signaling

2015-01-09 | GSE57985 | GEO

WNT11/ROR2 signaling is associated with tumor invasion and poor survival in breast cancer [patients]

Project description:Breast cancer is the most common cancer in women with more than two million new cases diagnosed in 2018. Patients frequently develop metastases in the course of their disease which limit survival due to the lack of a curative treatment. One signaling pathway that is frequently involved in cancer initiation and progression is the WNT pathway. Breast cancer has been associated with activation of the WNT signaling pathway, although the underlying molecular mechanisms are still unclear. Here, we found the WNT receptor ROR2 to be highly expressed in aggressive breast tumors and associated with worse metastasis-free survival. In this study we addressed this question and demonstrated for the first time that WNT11 is a novel ligand for ROR2 in humans. WNT11 binds to the CRD of ROR2 and mediates WNT/PCP signaling via the RHO/ROCK pathway that confers an aggressive phenotype to breast cancer cells. ROR2 and WNT11 are both highly expressed in human brain metastases and linked with short patient survival.

2022-02-21 | GSE161865 | GEO

iTRAQ-based quantitative proteomic analysis of nuclear proteome in VPS35-depleted HeLa cells

Project description:Stable VPS35 knockdown HeLa cells were generated using lentiviral short hairpin RNA (shRNA) construct. Isobaric tags for relative and absolute quantitation (iTRAQ)-based mass spectrometry was used to measure the changes of nuclear protein abundance in VPS35-depleted HeLa cells.

2022-08-12 | PXD027166 | Pride

Knockdown of Ror2 in lineage-depleted tumor cells were derived from 2153L basal-like TP53null mammary tumor models

Project description:Knockdown of Ror2 in lineage-depleted tumor cells were derived from 2153L basal-like TP53null mammary tumor models

| PRJNA734626 | ENA

Knock down effect of Ror2 on gene expression profiling in human osteosarcoma cells (SaOS2)

Project description:Ror2 is a member of the Ror-family of receptor tyrosine kinases acting as a receptor for Wnt5a. Wnt5a/Ror2 signaling activates primarily the ß-catenin-independent pathway, which involves various signal mediators, such as Dishevelled, c-Jun N-terminal kinase (JNK), filamin A, c-Src, and Ca2+. Wnt5a/Ror2 signaling has also been shown to inhibit the ß-catenin-dependent pathway. Wnt5a and Ror2 are overexpressed in various types of tumor cells, including osteosarcoma and melanoma cells, resulting in constitutive activation of Wnt5a/Ror2 signaling in a cell-autonomous manner. Constitutively activated Wnt5a/Ror2 signaling has been shown to play important roles in promoting invadopodia formation and invasiveness of tumor cells. However, little is known about the mechanisms underlying these processes. As an attempt to understand the mechanism by which Wnt5a/Ror2 signaling, activated constitutively in osteosarcoma cells, contributes to their highly invasive properties, we performed DNA microarray analysis using a human osteosarcoma cell line, SaOS2.

2017-01-01 | GSE76535 | GEO

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