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Neuronal mimicry mechanisms promote the growth small-cell lung cancer in the brain

ABSTRACT: Neuronal mimicry mechanisms promote the growth small-cell lung cancer in the brain

PROVIDER: PRJNA741987 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14930229.fastq.gz	Fastqsanger.gz
	SRR14930230.fastq.gz	Fastqsanger.gz
	SRR14930231.fastq.gz	Fastqsanger.gz
	SRR14930232.fastq.gz	Fastqsanger.gz
	SRR14930233.fastq.gz	Fastqsanger.gz

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Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain

Project description:Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain

| PRJNA740266 | ENA

Neuronal mimicry mechanisms promote the growth small-cell lung cancer in the brain

Project description:Small cell lung cancer (SCLC) is a fatal form of cancer that frequently metastasizes to the brain. Here we investigated the mechanisms allowing SCLC cells to grow in the unique brain microenvironment. We found that neuronal programs upregulated in SCLC cells during tumor progression and upon growth in the brain are critical for SCLC growth in the brain. Mechanistically, the presence of SCLC cells in the brain re-activates astrocytes, which in turn promote the survival of SCLC cells by secreting neuronal pro-survival factors such as SERPINE1. We also identified Reelin, a molecule produced by developing neurons to recruit astrocytes, as a molecule secreted by SCLC cells to recruit astrocytes to the tumor site and promote SCLC growth in the brain. Thus, SCLC cells co-opt mechanisms normally at play between astrocytes and neurons to promote SCLC growth in the brain. Targeting such developmental neuronal programs may help treat brain metastases.

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Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human astrocytes RNA-seq]

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Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human astrocytes RNA-seq]

Project description:Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human astrocytes RNA-seq]

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Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [TA and CA RNA-seq]

2023-08-09 | GSE178732 | GEO

Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [TA and CA RNA-seq]

Project description:Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [TA and CA RNA-seq]

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Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human SCLC cell RNA seq]

Project description:Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain [human SCLC cell RNA seq]

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Neuronal mimicry mechanisms promote the growth of small-cell lung cancer in the brain

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

2023-08-09 | GSE178743 | GEO

Chronic viral mimicry induction following p53 loss promotes immune evasion [scRNASeq]

Project description:Epigenetic therapies that alter DNA- and/or histone modifications facilitate transcription of immunogenic repetitive elements that cull cancer cells through ‘viral mimicry’ responses. Paradoxically, cancer-initiating events that include functional inactivation of canonical tumor suppressor proteins also facilitate transcription of repetitive elements. Contributions of repetitive element transcription towards cancer initiation, and the mechanisms by which cancer cells evade lethal viral mimicry responses during tumor initiation remain poorly understood. In this report, we characterize patient-derived premalignant lesions of the fallopian tube along with syngeneic mouse models of epithelial ovarian cancer to explore the earliest events of tumorigenesis following loss of the p53 tumor suppressor protein. We report that p53 loss disrupts constitutive heterochromatin to permit transcription of immunogenic repetitive elements capable of activating viral mimicry responses. While acute viral mimicry activation diminishes cell fitness, chronic viral mimicry activation following p53 loss promotes epigenetic reprogramming that increases tolerance of cytosolic nucleic acids and diminishes cellular immunogenicity as a pro-survival adaptation. This selection process we describe as ‘viral mimicry conditioning’ can be partially attenuated by the reverse transcriptase inhibitor 3TC to delay spontaneous tumorigenesis. Altogether, these results reveal that viral mimicry conditioning following p53 loss selects for diminished cell immunogenicity to promote immune evasion upon cancer initiation. Disruption of viral mimicry conditioning during cancer initiation may represent a pharmacological target for early cancer interception.

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