Immunoprofiling of mouse prostate cancer infiltrate
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA958227 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24258300.fastq.gz | Fastqsanger.gz | |||
| SRR24258301.fastq.gz | Fastqsanger.gz | |||
| SRR24258302.fastq.gz | Fastqsanger.gz | |||
| SRR24258303.fastq.gz | Fastqsanger.gz | |||
| SRR24258304.fastq.gz | Fastqsanger.gz |
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Project description:Immunoprofiling of prostate cancer infiltrate
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Project description:The development of autonomic nerve fibres in the tumour microenvironment is a pivotal event that regulates prostate cancer initiation and dissemination, but how nerves emerge in tumours is presently unknown. Here we show that Doublecortine-expressing (DCX+) neural precursors from the central nervous system (CNS) infiltrate prostate tumours and differentiate into neo-neurons that contribute to tumour development. In human primary prostate tumours and transgenic mouse cancer tissues, the density of DCX+ neural progenitors is strongly associated with tumour aggressiveness, invasion and recurrence. We found that DCX+ neural precursors egress from the subventricular zone, a neurogenic area of the CNS, and circulate in the blood to reach the tumour where they initiate neurogenesis. Hence, the DCX+ cells in prostate tumour can differentiate into neurons ex vivo and build up a tumour-associated neural network in vivo. Selective genetic depletion of DCX+ cells in mice significantly inhibits the early phases of prostate cancer development, whereas orthotopic transplantation of DCX+ cells purified from prostate tumour or brain tissues promotes tumour growth and cancer cell dissemination. These results unveil a unique crosstalk between the CNS and the tumour that drives a process of neurogenesis necessary for prostate cancer development, and indicate a novel neural element of the tumour microenvironment as a potential target for cancer treatment.
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Project description:Yap1 is a critical transcription coactivator in the Hippo pathways. However, its target genes are not well defined in prostate cancer cells. To determine the downstream transcriptional targets and pathways of Yap1 in Pten/Smad4-defiicent mouse prostate cancer cells, ChIP-seq was performed in the Pten/Smad4-deficient mouse prostate cancer cells.
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