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

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

PROVIDER: PRJNA734626 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14713182_1.fastq.gz	Fastqsanger.gz
	SRR14713182_2.fastq.gz	Fastqsanger.gz
	SRR14713183_1.fastq.gz	Fastqsanger.gz
	SRR14713183_2.fastq.gz	Fastqsanger.gz
	SRR14713184_1.fastq.gz	Fastqsanger.gz

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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.

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

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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

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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.

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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.

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

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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.

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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.

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Project description:Mouse mammary tumors are diverse neoplastic growths originating in the mammary glands of mice and serve as essential models for studying human breast cancer. These tumors can be classified into distinct molecular subtypes, including luminal, basal-like, HER2-enriched, and claudin-low, reflecting the heterogeneity observed in breast cancer. With unique genetic and molecular features, these subtypes are instrumental for understanding the complexities of tumor biology. Here we sequenced the mRNA of 13 treatment-na ve mouse mammary tumor lines for a total of 82 samples.

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Expression and role of the receptor tyrosine kinase-like orphan receptor2 (ROR2) in small cell lung cancer

Project description:Heterogeneity of ROR2 was observed in the tumor tissues form patient-derived xenograft (PDX) model of SCLC, in which the cells with high ROR2 expression (ROR2high cell) and those without ROR2 expression (ROR2low cell) were gained and subjected to RNA sequence analysis. Cell proliferation activity was suppressed in ROR2 KO SBC3 cells in vitro and in vivo. Comparison of the downregulated DEG in the ROR2 KO SBC3 cells and the upregulated DEG in ROR2high cells in the PDX model revealed 135 common genes. After Metascape analysis of these genes, we focus on Aurora kinases. These results suggest that ROR2 could regulate cell cycle through AURKA and/or AURKB. This study clarrifies the function of ROR2 in SCLC with heterogeneous expression condition.

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