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Nociceptor neurons affect cancer immunosurveillance [RNA-seq 2]

ABSTRACT: Sequencing Neuron, melanoma and CD8 when culture alone or co-culture with one another

ORGANISM(S): Mus musculus

PROVIDER: GSE205864 | GEO | 2022/08/10

REPOSITORIES: GEO

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Nociceptor neurons affect cancer immunosurveillance [RNA-seq 1]

Project description:Neuron, melanoma and CD8 co-cultures

2022-08-10 | GSE205863 | GEO

Nociceptor neurons affect cancer immunosurveillance.

Project description:Solid tumours are innervated by nerve fibres that arise from the autonomic and sensory peripheral nervous systems1-5. Whether the neo-innervation of tumours by pain-initiating sensory neurons affects cancer immunosurveillance remains unclear. Here we show that melanoma cells interact with nociceptor neurons, leading to increases in their neurite outgrowth, responsiveness to noxious ligands and neuropeptide release. Calcitonin gene-related peptide (CGRP)-one such nociceptor-produced neuropeptide-directly increases the exhaustion of cytotoxic CD8+ T cells, which limits their capacity to eliminate melanoma. Genetic ablation of the TRPV1 lineage, local pharmacological silencing of nociceptors and antagonism of the CGRP receptor RAMP1 all reduced the exhaustion of tumour-infiltrating leukocytes and decreased the growth of tumours, nearly tripling the survival rate of mice that were inoculated with B16F10 melanoma cells. Conversely, CD8+ T cell exhaustion was rescued in sensory-neuron-depleted mice that were treated with local recombinant CGRP. As compared with wild-type CD8+ T cells, Ramp1-/- CD8+ T cells were protected against exhaustion when co-transplanted into tumour-bearing Rag1-deficient mice. Single-cell RNA sequencing of biopsies from patients with melanoma revealed that intratumoral RAMP1-expressing CD8+ T cells were more exhausted than their RAMP1-negative counterparts, whereas overexpression of RAMP1 correlated with a poorer clinical prognosis. Overall, our results suggest that reducing the release of CGRP from tumour-innervating nociceptors could be a strategy to improve anti-tumour immunity by eliminating the immunomodulatory effects of CGRP on cytotoxic CD8+ T cells.

| S-EPMC9646485 | biostudies-literature

Nociceptor neurons affect cancer immunosurveillance

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

2022-08-10 | GSE205866 | GEO

Nociceptor neurons affect cancer immunosurveillance

Project description:Nociceptor neurons affect cancer immunosurveillance

| PRJNA847963 | ENA

Nociceptor neurons affect cancer immunosurveillance [RNA-seq 3]

Project description:Sequecing tumor-innervating neurons

2022-08-10 | GSE205865 | GEO

Nociceptor neurons affect cancer immunosurveillance [RNA-seq 3]

Project description:Nociceptor neurons affect cancer immunosurveillance [RNA-seq 3]

| PRJNA847968 | ENA

Nociceptor neurons affect cancer immunosurveillance [RNA-seq 2]

Project description:Nociceptor neurons affect cancer immunosurveillance [RNA-seq 2]

| PRJNA847969 | ENA

Nociceptor neurons affect cancer immunosurveillance [RNA-seq 1]

Project description:Nociceptor neurons affect cancer immunosurveillance [RNA-seq 1]

| PRJNA847967 | ENA

Characterization of melanoma cells exposed to melanoma-specific CD8+ T cells

Project description:Human low passage melanoma cell lines were compared after 24h culture alone or in presence of melanoma-specific CD8+ T cell clones

2016-08-30 | GSE79991 | GEO

Linking immortalization to direct conversion of human fibroblasts to neurons

Project description:Direct conversion from fibroblasts to neurons is a potential cell replacement therapy for neurological disorders, and a variety of combinations of transcription factors have been tried. We notice that the efficiency of conversion from aging fibroblasts was much lower than in early stage cells, which is consistent with the notion that cellular senescence impairs conversion of fibroblasts to neurons. Here, we found that the transient knockdown of the p16Ink4a/p19Arf locus was sufficient to convert human fibroblasts to neurons. Futhermore, expression of hTERT alone, another mechanism behind immortalization, also induced neuron conversion. Our results show that the acquisition of immortality is a crucial step for the conversion of human fibroblasts into induced neurons. Transient knockdown of p16/p19 or p53 expression or exogenous overexpression of hTERT can induce primary fibroblasts to immortality. In the following, treated cells were cultured in neuron-induction medium. We can observe the morphology change and detect the neuronal markers. Also, some of the induced neurons could generate action potentials and neurotransmitter-induced currents in optimal conditions.

2012-12-28 | E-GEOD-43175 | biostudies-arrayexpress

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