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Reelin-LRP8 signaling mediates brain metastasis of breast cancer cells via abluminal migration

ABSTRACT: Reelin-LRP8 signaling mediates brain metastasis of breast cancer cells via abluminal migration

PROVIDER: PRJNA1221936 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32300992_1.fastq.gz	Fastqsanger.gz
	SRR32300992_2.fastq.gz	Fastqsanger.gz
	SRR32300993_1.fastq.gz	Fastqsanger.gz
	SRR32300993_2.fastq.gz	Fastqsanger.gz
	SRR32300994_1.fastq.gz	Fastqsanger.gz

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Reelin-LRP8 signaling mediates brain metastasis of breast cancer cells via abluminal migration

Project description:Brain metastasis (BM) remains a significant challenge in breast cancer (BC) management. While conventional metastatic routes involve hematogenous dissemination, emerging evidence suggests that BC cells can also migrate along the abluminal surface of blood vessels, bypassing the blood-brain barrier (BBB). To investigate this phenomenon, we established a zebrafish xenograft model utilizing GFP-labeled MDA-MB-231 cells, allowing real-time observation of BC cell migration along the posterior cerebral veins. Our findings revealed that LRP8, a apolipoprotein E receptor, is upregulated in BC patients with brain metastases. Functional studies demonstrated that LRP8 knockdown significantly inhibited proliferation, migration, and invasion of triple-negative breast cancer (TNBC) cells both in vitro and in vivo. Mechanistically, LRP8 promotes the activation of CDC42, enhancing filopodia formation and cell motility, a process influenced by the neuronal extracellular matrix protein, Reelin. Furthermore, we demonstrate the therapeutic potential of MEN 10207, a neurokinin-2 receptor antagonist, in inhibiting TNBC cell migration and suppressing BM formation in both zebrafish and mouse models. These findings provide novel insights into the mechanisms underlying extravascular brain metastasis in BC, highlighting the Reelin-LRP8-CDC42 axis as a potential therapeutic target for this devastating complication.

2025-05-22 | GSE289226 | GEO

LRP8-Reelin-regulated Neuronal (LRN) Enhancer signature underlying learning and memory formation (RNA-Seq 1)

Project description:A comprehensive landscape of epigenomic events regulated by the Reelin signaling through activation of specific cohort of cis-regulatory enhancer elements (LRN-enhancers), which involves the proteolytical processing of the LRP8 receptor by the gamma-secretase activity and is required for learning and memory behavior All RNA-Seq experiments were designed to evaluate the transcriptional program regulated by the Reelin-LRP8 signaling pathway in neuronal cells

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LRP8-Reelin-regulated Neuronal (LRN) Enhancer signature underlying learning and memory formation (RNA-Seq 2)

2015-04-29 | E-GEOD-66707 | biostudies-arrayexpress

Nonsense-mediated mRNA decay orchestrates neuronal migration and cortical lamination while modulating reelin and ciliary gene regulatory networks (RNAseq)

Project description:Nonsense-mediated mRNA decay (NMD) is associated with various neurodevelopmental disorders. Here, we demonstrate that NMD, mediated by UPF2, previously not linked to cortical organization, is indispensable for neuronal migration and cortical lamination. Conditional deletion of Upf2 in radial glial cells delays neuronal migration and disrupts cortical lamination. Trp53 knockout rescues microcephaly from Upf2 deficiency but cannot rescue lamination defects, showing that UPF2’s role in neuronal migration is uncoupled from its regulation of cell cycle and independent of p53. UPF2 deficiency downregulates key neuronal migration genes in the Reelin signaling pathway and microtubule assembly (e.g., Dab1, Lrp8, Tubb2b, Tuba1a), partly through upregulation of the transcriptional repressor Ino80. Additionally, NMD inhibition causes widespread upregulation of ciliary genes. Ectopic expression of Foxj1, a master regulator of ciliary genes and NMD target, impedes neuronal migration, mimicking the Upf2 knockout phenotype. Therefore, NMD is a central post-transcriptional mechanism that coordinates migration and ciliary gene networks crucial for cortical structure development, providing insight into how NMD dysfunction contributes to neurodevelopmental disorders.

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Nonsense-mediated mRNA decay orchestrates neuronal migration and cortical lamination while modulating reelin and ciliary gene regulatory networks (snRNAseq)

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LRP8-Reelin-regulated Neuronal (LRN) Enhancer signature underlying learning and memory formation (GRO-seq)

Project description:A comprehensive landscape of epigenomic events regulated by the Reelin signaling through activation of specific cohort of cis-regulatory enhancer elements (LRN-enhancers), which involves the proteolytical processing of the LRP8 receptor by the gamma-secretase activity and is required for learning and memory behavior All GRO-Seq experiments were designed to understand the unique signature of LRN-enhancers and to evaluate the transcriptional response to Reelin treatment in neuronal cells.

2015-04-29 | E-GEOD-66703 | biostudies-arrayexpress