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Ror2-mediated non-canonical Wnt signaling regulates Cdc42 and cell proliferation during root development

ABSTRACT: Ror2-mediated non-canonical Wnt signaling regulates Cdc42 and cell proliferation during root development

PROVIDER: PRJNA678015 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13051335.fastq.gz	Fastqsanger.gz
	SRR13051336.fastq.gz	Fastqsanger.gz
	SRR13051337.fastq.gz	Fastqsanger.gz
	SRR13051338.fastq.gz	Fastqsanger.gz
	SRR13051339.fastq.gz	Fastqsanger.gz

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Ror2-mediated non-canonical Wnt signaling regulates Cdc42 and cell proliferation during root development

Project description:We show that Ror2 mediated non-canonical Wnt signaling in the dental mesenchyme plays a critical role in cell proliferation and thereby regulates root development size in mouse molars. Furthermore, Cdc42 acts as a potential downstream mediator of Ror2 signaling in root formation.

2020-11-13 | GSE161395 | GEO

Non-canonical Wnt signaling via FZD5 and ROR2 contributes to the maintenance of the stemness of human mesenchymal stem cells

Project description:We previously showed that the combination of markers LNGFR+ and THY-1+ can be used selectively to isolate human mesenchymal stem cells (hMSCs) in bone marrow and several tissues. However, the molecular mechanisms regulating stemness of hMSCs remain to be elucidated. In this study, we found that Frizzled 5 (FZD5) and Receptor tyrosine kinase-like orphan receptor 2 (ROR2) were highly enriched in LNGFR+THY-1+ derived clones that retain a high potential for proliferation (rapidly expanding clones; RECs). WNT5A, the ligand of FZD5, causes FZD5 and ROR2 to co-localize and activates non-canonical Wnt pathway in RECs. Moreover, FZD5 knockdown attenuated proliferation and caused senescence. In contrast, FZD5 overexpression delayed senescence. These results indicate that intrinsic activation of non-canonical Wnt signaling via FZD5 and ROR2 modulates stemness and senescence of RECs. Thus, control of non-canonical Wnt signaling would enable us to regulate hMSC quality and to enhance the efficacy of cell-replacement therapy using hMSCs.

2016-09-02 | GSE86369 | GEO

Gene expression profiling comparing myeloma cell line MM1.144 transduced with a scramble shRNA or an shRNA targeting the non-canonical WNT receptor ROR2

Project description:We examined the gene expression profiles resulting from the depletion of the non-canonical WNT receptor ROR2 in myeloma cells

2019-07-22 | GSE118040 | GEO

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

A DLG1-ARHGAP31-CDC42 axis regulates the Wnt response in intestinal stem cells

Project description:A central factor in maintenance of tissue integrity is the response of stem cells to variations in the levels of niche signals. In the gut, intestinal stem cells (ISCs) depend on Wnt ligands for self-renewal and proliferation. Transient increases in Wnt signaling promote regeneration after injury or in inflammatory bowel diseases, whereas constitutive activation of this pathway leads to colorectal cancer. Here, we report that Discs large 1 (Dlg1) is dispensable for polarity and cellular turnover during intestinal homeostasis; however, Dlg1 is required for ISC survival in the context of increased Wnt signaling. RNA sequencing (RNAseq) and genetic mouse models demonstrated that DLG1 regulates the cellular response to increased canonical Wnt signaling. This occurs via transcriptional regulation of Arhgap31, a GTPase-activating protein that deactivates CDC42, an effector of the non-canonical Wnt pathway. These findings reveal a DLG1-ARHGAP31-CDC42 axis that is essential for the ISC response to fluctuating niche Wnt signaling.

2023-01-15 | GSE198573 | GEO

Targets of ROR2 overexpression in MCF-7 cells revealed a differentially regulated module of non-canonical WNT signaling pathway

Project description:RNA-Seq profiling of estrogen-receptor-positive MCF-7 cell lines with different perturbations of non-canonical WNT signaling . The MCF-7 cells were either transfected with an empty vector (pcDNA) or with a ROR2 overexpression construct, in parallel with or without stimulation with recombinant WNT5A. The objective was to find expression-responsive targets of these perturbations as potential drivers of increased cell invasiveness.

2017-08-17 | GSE74383 | GEO

Ror2-mediated non-canonical Wnt signaling regulates Cdc42 and cell proliferation during tooth root development.

Project description:The control of size and shape is an important part of regulatory process during organogenesis. Tooth formation is a highly complex process that fine-tunes the size and shape of the tooth, which are crucial for its physiological functions. Each tooth consists of a crown and one or more roots. Despite comprehensive knowledge of the mechanism that regulates early tooth crown development, we have limited understanding of the mechanism regulating root patterning and size during development. Here, we show that Ror2-mediated non-canonical Wnt signaling in the dental mesenchyme plays a crucial role in cell proliferation, and thereby regulates root development size in mouse molars. Furthermore, Cdc42 acts as a potential downstream mediator of Ror2 signaling in root formation. Importantly, activation of Cdc42 can restore cell proliferation and partially rescue the root development size defects in Ror2 mutant mice. Collectively, our findings provide novel insights into the function of Ror2-mediated non-canonical Wnt signaling in regulating tooth morphogenesis, and suggest potential avenues for dental tissue engineering.

| S-EPMC7847279 | biostudies-literature

WNT7 Promotes Proliferation of Pancreatic Progenitor Cells Differentiated from Human Pluripotent Stem Cells through Non-Canonical Wnt Signaling Pathway

Project description:A small molecule, AT7867, promotes proliferation of human pluripotent stem cell-derived pancreatic progenitor cells (PPCs), yet detailed mechanisms of its proliferative effect were not fully understood. Here, we performed cell-based siRNA screening on a subset of genes to reveal that WNT7B is a growth factor of human PPCs as previously shown in mouse pancreas development. Although recombinant proteins had no in vitro activity, feeder cell lines stably expressing Wnt7a or Wnt7b enhanced PPC proliferation. Further analyses showed that canonical Wnt signaling pathway was not affected by AT7867 treatment as well as Wnt7a and Wnt7b. Knockdown of a non-canonical Wnt pathway component, PKCα, and its downstream substrate, MARCKS, blocked PPC proliferation suggesting a requirement of this pathway. Phosphoproteome analysis revealed that AT7867 inhibited Yin Yang 1 (YY1) phosphorylation at Ser118, which directly or indirectly regulated expression of WNT7B in PPCs. Taken together, non-canonical Wnt signaling mediated by WNT7B plays a critical role for the expansion of human PPC population that is a promising alternative cell source to generate β cells for the cure of diabetes.

2021-07-01 | PXD018221 | JPOST Repository

WNT7 Promotes Proliferation of Pancreatic Progenitor Cells Differentiated from Human Pluripotent Stem Cells through Non-Canonical Wnt Signaling Pathway

2022-03-27 | PXD018222 | JPOST Repository

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

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