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Neuropilin-2 axis in regulating secretory phenotype of neuroendocrine-like prostate cancer cells: implication in therapy resistance

ABSTRACT: Neuropilin-2 axis in regulating secretory phenotype of neuroendocrine-like prostate cancer cells: implication in therapy resistance

PROVIDER: PRJNA835419 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19095642_1.fastq.gz	Fastqsanger.gz
	SRR19095642_2.fastq.gz	Fastqsanger.gz
	SRR19095643_1.fastq.gz	Fastqsanger.gz
	SRR19095643_2.fastq.gz	Fastqsanger.gz
	SRR19095644_1.fastq.gz	Fastqsanger.gz

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Neuropilin-2 axis in regulating secretory phenotype of neuroendocrine-like prostate cancer cells: implication in therapy resistance

Project description:Gene expression was first compared between prostate adenocarcinoma cell line LNCaP C4-2 and our developed neuroendocrine like derived cell line DKD (LNCaP C4-2 stably depleted with TP53 and RB1). In the next set, we compared the gene expression of neuroendocrine like DKD under presence and absence of Neurolipilin-2.

2022-05-09 | GSE202299 | GEO

Neuropilin-2 axis in regulating secretory phenotype of neuroendocrine-like prostate cancer cells and its implication in therapy resistance.

Project description:Neuroendocrine (NE)-like tumors secrete various signaling molecules to establish paracrine communication within the tumor milieu and to create a therapy-resistant environment. It is important to identify molecular mediators that regulate this secretory phenotype in NE-like cancer. The current study highlights the importance of a cell surface molecule, Neuropilin-2 (NRP2), for the secretory function of NE-like prostate cancer (PCa). Our analysis on different patient cohorts suggests that NRP2 is high in NE-like PCa. We have developed cell line models to investigate NRP2's role in NE-like PCa. Our bioinformatics, mass spectrometry, cytokine array, and other supporting experiments reveal that NRP2 regulates robust secretory phenotype in NE-like PCa and controls the secretion of factors promoting cancer cell survival. Depletion of NRP2 reduces the secretion of these factors and makes resistant cancer cells sensitive to chemotherapy in vitro and in vivo. Therefore, targeting NRP2 can revert cellular secretion and sensitize PCa cells toward therapy.

| S-EPMC9362995 | biostudies-literature

Neuropilin-2 Promotes the Development of Neuroendocrine Prostate Cancer

Project description:Neuropilin-2 Promotes the Development of Neuroendocrine Prostate Cancer

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Neuropilin-1+ vs. Neuropilin-1- CD8+ T cells from Plasmodium berghei ANKA-infected mice

Project description:Characterization of Neuropilin-1+ and Neuropilin-1- splenic CD8+ T cells from Plasmodium berghei ANKA-infected C57BL/6 mice

2022-12-31 | GSE199569 | GEO

Neuropilin-1+ vs. Neuropilin-1- CD8+ T cells from Plasmodium berghei ANKA-infected mice

Project description:Neuropilin-1+ vs. Neuropilin-1- CD8+ T cells from Plasmodium berghei ANKA-infected mice

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Neuropilin-1 is Required for the Suppressive Function of Human Regulatory T Cells

Project description:Regulatory T cells (Tregs), lymphocytes that suppress immunological reactions, are of great interest for our comprehension of homeostasis and regulation in the immune system and as a therapeutic target in the treatment of both immune-mediated pathologies and reactivation of the immune response in patients with cancer. Understanding the molecular mechanisms by which these cells are regulated in respone to their environment will help to inform clinical strategies targeting Tregs. We hypothesised that Neuropilin-1, a transmembrane co-receptor for ligands of the semaphorin and growth factor families, promotes the suppressive function of human Tregs. Utilising in vitro lentivirus-mediated transduction with shRNA to knock down neuropilin-1 in primary human Tregs, we demonstrated that neuropilin-1 knockdown Tregs were severely impaired in their capacity to suppress cell proliferation in vitro and in their ability to prolong allograft survival in a humanised mouse model of transplantation. While neuropilin-1-KD Tregs exhibited no defects in survival, proliferation and activation upon stimulation in vitro, we hypothesised that loss of NRP1 expression would alter the global gene expression profile of human Tregs, revealing a NRP1-dependent Treg-associated transcriptional signature.

2019-01-01 | GSE106932 | GEO

Neuropilin 1 interactome in endothelial cells

Project description:To get unbiased insights on the molecular networks through by which Neuropilin 1 (NRP1) controls endothelial cell (EC) and blood vessel functions independently from its ligands, wehave implemented a Halo Tag (HT)-based approach, which enables effective surface labeling and pull-down of proteins, and combined it with quantitative mass spectrometry (MS) analysis.

2022-06-15 | PXD019700 | Pride

ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype

Project description:ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype

2020-04-03 | MSV000085224 | MassIVE

Role of Neuropilin-1 in regulatory T cell stability and function

Project description:To investigate the function of Neuropilin-1 (NRP-1) in Foxp3+ regulatory T (Treg) cell stability and function, we cultured naïve CD4+ T cells under induced Treg cell (iTreg)-differentiating condition. We then flow sorted NRP-1+ and NRP-1- iTreg cells and performed gene expression profiling analysis.

2022-04-30 | GSE201416 | GEO

Genome-wide features of neuroendocrine regulation in Drosophila by the basic helix-loop-helix transcription factor DIMMED

Project description:Neuroendocrine (NE) cells use large dense core vesicles (LDCVs) to traffic, process, store and secrete neuropeptide hormones through the regulated secretory pathway. The DIMM basic helix-loop-helix transcription factor of Drosophila controls the level of regulated secretory activity in NE cells. To pursue its mechanisms, we have performed two independent genome-wide analyses of DIMMM-bM-^@M-^Ys activities: (i) in vivo chromatin immunoprecipitation (ChIP) to define genomic sites of DIMM occupancy and (ii) deep sequencing of purified DIMM neurons to characterize their transcriptional profile. By this combined approach, we showed that DIMM binds to conserved E-boxes in enhancers of 212 genes whose expression is enriched in DIMM-expressing NE cells. DIMM binds preferentially to certain E-boxes within first introns of specific gene isoforms. Statistical machine learning revealed that flanking regions of putative DIMM binding sites contribute to its DNA binding specificity. DIMMM-bM-^@M-^Ys transcriptional repertoire features at least 20 LDCV constituents. In addition, DIMM notably targets the pro-secretory transcription factor, CREB-A, but significantly, DIMM does not target any neuropeptide genes. DIMM therefore prescribes the scale of secretory activity in NE neurons, by a systematic control of the regulated secretory pathway at steps that are both proximal and distal. DIMM::MYC ChIP-chip (c929>DIMM::MYC/tubGAL80ts) and control (c929>tubGAL80ts): 2 replicates each, input and IP samples. Total of 8 arrays

2015-02-02 | E-GEOD-65512 | biostudies-arrayexpress

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