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Notch signaling suppresses neuroendocrine differentiation and alters the tumor immune microenvironment in advanced prostate cancer

ABSTRACT: Notch signaling suppresses neuroendocrine differentiation and alters the tumor immune microenvironment in advanced prostate cancer

PROVIDER: PRJNA983287 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24911703_1.fastq.gz	Fastqsanger.gz
	SRR24911703_2.fastq.gz	Fastqsanger.gz
	SRR24911704_1.fastq.gz	Fastqsanger.gz
	SRR24911704_2.fastq.gz	Fastqsanger.gz
	SRR24911705_1.fastq.gz	Fastqsanger.gz

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Notch signaling suppresses neuroendocrine differentiation and alters the tumor immune microenvironment in advanced prostate cancer

Project description:Neuroendocrine prostate cancer (NEPC) is an aggressive, androgen-independent variant of prostate cancer (PCa) that most commonly develops in patients as a mechanism of therapeutic resistance. The underlying mechanisms driving PCa lineage plasticity and trans-differentiation to a neuroendocrine lineage are not fully understood. Here, we identify Notch signaling as a key suppressor of neuroendocrine differentiation in PCa. Restoration of Notch signaling in NEPC models results in phenotypic conversion towards a non-neuroendocrine state with expression of prostate luminal cell markers and immunologic changes including up-regulation of MHC Class I and II and type I interferon signaling that correlate with changes in the tumor immune microenvironment. Overall, these data provide new insights into how Notch signaling influences PCa lineage plasticity and points to new therapeutic avenues to modulate it.

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Notch signaling suppresses neuroendocrine differentiation and alters the tumor immune microenvironment in advanced prostate cancer

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Notch signaling suppresses neuroendocrine differentiation and alters the tumor immune microenvironment in advanced prostate cancer

Project description:Notch signaling suppresses neuroendocrine differentiation and alters the tumor immune microenvironment in advanced prostate cancer

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Notch signaling suppresses neuroendocrine differentiation and alters the immune microenvironment in advanced prostate cancer.

Project description:Notch signaling can have either an oncogenic or tumor-suppressive function in cancer depending on the cancer type and cellular context. While Notch can be oncogenic in early prostate cancer, we identified significant downregulation of the Notch pathway during prostate cancer progression from adenocarcinoma to neuroendocrine (NE) prostate cancer, where it functions as a tumor suppressor. Activation of Notch in NE and Rb1/Trp53-deficient prostate cancer models led to phenotypic conversion toward a more indolent, non-NE state with glandular features and expression of luminal lineage markers. This was accompanied by upregulation of MHC and type I IFN and immune cell infiltration. Overall, these data support Notch signaling as a suppressor of NE differentiation in advanced prostate cancer and provide insights into how Notch signaling influences lineage plasticity and the tumor microenvironment (TME).

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A conserved YAP/Notch/REST network controls the neuroendocrine cell fate in the lungs [ChIP-seq]

Project description:The Notch pathway is a conserved cell-cell communication pathway that controls cell fate decisions. Here we sought to determine how Notch pathway activation inhibits the neuroendocrine cell fate in the lungs, an archetypal process for cell fate decisions orchestrated by Notch signaling that has remained poorly understood at the molecular level. Using heterogeneity in small cell lung cancer as a model system, we uncovered a role for the transcriptional regulators REST and YAP as promoters of the neuroendocrine to non-neuroendocrine transition. We further identified the specific neuroendocrine gene programs repressed by REST downstream of Notch in this process. Importantly, we validated the importance of REST and YAP in neuroendocrine to non-neuroendocrine cell fate switches in both developmental and tissue repair processes in the lungs. Altogether, these experiments identify conserved roles for REST and YAP in Notch-driven inhibition of the neuroendocrine cell fate in embryonic lungs, adult lungs, and lung cancer.

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