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CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration

ABSTRACT: CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration

PROVIDER: PRJNA994561 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25268919.fastq.gz	Fastqsanger.gz
	SRR25268919_1.fastq.gz	Fastqsanger.gz
	SRR25268919_2.fastq.gz	Fastqsanger.gz
	SRR25268920.fastq.gz	Fastqsanger.gz
	SRR25268920_1.fastq.gz	Fastqsanger.gz

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CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [I]

Project description:Brain metastasis of lung cancer causes high mortality, but the exact mechanisms underlying the metastasis remain unclear. Here we report that vascular pericytes derived from CD44+ lung cancer stem cells (CSCs) in lung adenocarcinoma (ADC) potently cause brain metastases through GPR124-mediated trans-endothelial migration (TEM). CD44+ CSCs in the perivascular niche generate the majority of vascular pericytes in lung ADC. CSC-derived pericyte-like cells (Cd-pericytes) exhibit remarkable TEM capacity to effectively intravasate into vessel lumina, survive in the circulation, extravasate into the brain parenchyma, and then de-differentiate into tumorigenic CSCs to form metastases. Moreover, Cd-pericytes uniquely express GPR124, a G-protein-coupled receptor. GPR124 mediates through Wnt7-β-Catenin activation to enhance TEM capacity of Cd-pericytes for intravasation and extravasation, two critical steps during tumor metastasis. Furthermore, selective disruption of Cd-pericytes, GPR124 or Wnt7-β-Catenin signaling markedly reduced brain and liver metastases of lung ADC. Our findings uncover an unappreciated cellular and molecular paradigm driving tumor metastasis.

2023-07-23 | GSE237316 | GEO

CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [II]

2023-07-23 | GSE237317 | GEO

CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [II]

Project description:CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [II]

| PRJNA994564 | ENA

CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [I]

Project description:CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration [I]

| PRJNA994565 | ENA

CD44+ Lung Cancer Stem Cell-derived Vascular Pericytes Cause Brain Metastases through GPR124-mediated Trans-endothelial Migration

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

2023-07-23 | GSE237319 | GEO

GPR124 Protects against Podocyte Senescence and Injury in Diabetic Kidney Disease

Project description:Cellular senescence is associated with the progression of diabetic kidney disease (DKD), and accelerated podocyte senescence promotes the pathogenesis of renal damage. We found that GPR124 was reduced in cultured human podocytes treated with high glucose (HG).To further clarify the role of GPR124 in podocytes, we overexpressed GPR124 via plasmid-harboring adenovirus infection. By RNA sequencing analysis of podocytes with different treatment, we observed GPR124 overexpression significantly affected several kinds of cell adhesion.

2024-11-05 | GSE280773 | GEO

GPR124 regulates murine CNS angiogenesis and blood-brain barrier formation by an intracellular domain-independent mechanism

Project description:The GPR124/RECK/WNT7 pathway essentially regulates central nervous system angiogenesis and blood-brain barrier (BBB) function. GPR124, a brain endothelial adhesion 7-pass transmembrane protein, associates with membrane RECK, which binds and stabilizes newly synthesized WNT7 for subsequent transfer to Frizzled (FZD) and canonical b-catenin signaling. GPR124 function remains enigmatic; while its extracellular domain (ECD) is required, the poorly conserved intracellular domain (ICD) appears to be variably required in mammals versus zebrafish, potentially mediated by bridging of the GPR124 and FZD ICDs by intracellular adaptor proteins. GPR124 ICD deletion mutants impair zebrafish angiogenesis, but paradoxically still mediate WNT7 signaling upon mammalian cell transfection. We thus further investigated the GPR124 C-terminal ICD by deletion in mice (Gpr124ΔC). Notably, Gpr124ΔC/ΔC mice could be born and did not recapitulate Gpr124-/- embryonic lethal forebrain hemorrhage. GPR124ΔC protein was inefficiently expressed, resulting in mild, hypomorphic, non-hemorrhagic defects in CNS angiogenesis and BBB function, sparing the cortex and only confined to ganglionic eminences. Impaired surface expression of GPR124ΔC directly correlated with reduced endothelial WNT signaling, arguing against an intrinsic signaling deficiency. Further, GPR124ΔC and recombinant GPR124 ECD both rescued WNT7 signaling following brain endothelial Gpr124 knockdown. Thus, in mice, the GPR124 essential regulation of WNT7-dependent CNS forebrain angiogenesis and BBB function is exerted by ICD-independent functionality, extending the range of signaling mechanisms used by adhesion 7-pass transmembrane receptors.

2024-04-19 | GSE225367 | GEO

Gpr124 is essential for blood-brain barrier integrity in central nervous system disease

Project description:Although blood-brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined. The endothelial G protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adults is unknown. Here, conditional Gpr124 knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity but resulted in BBB disruption and microvascular hemorrhage in mouse models of ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt/beta-catenin signaling. Constitutive activation of Wnt/beta-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124 cko mice, with rescue of the endothelial tight junction, pericyte coverage and extracellular-matrix deficits. We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice. This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption.

2017-03-06 | GSE74052 | GEO

Proteomic data for tumor pericytes with TCFA2 overexpression

Project description:This study aims to investigate differentially expressed proteins in tumor pericytes with or without TCAF2-ovexpression. Tumor pericytes were isolated from tumor of patients with colorectal cancer. Then, tumor pericytes were cultured, transfected with vector or TCAF2 overexpressing plasmid. Top ten cytokines were screened and Wnt5a was the most significant one.

2024-01-26 | PXD032935 | Pride

Proteomic data for tumor pericytes derived from colorectal cancer patients

Project description:This study aims to investigate differentially expressed proteins in tumor pericytes derived from colorectal cancer patients with or without liver metastasis. Tumor pericytes were isolated from tumor of colorectal cancer patients with or without liver metastasis. Then, tumor pericytes were cultured and subjected to proteomic analysis. TCAF2 was significantly increased in tumor pericytes from liver metastasis patients.

2024-01-26 | PXD033011 | Pride

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