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Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [RNA-seq]

ABSTRACT: Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [RNA-seq]

PROVIDER: PRJNA431975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6518480.fastq.gz	Fastqsanger.gz
	SRR6518490.fastq.gz	Fastqsanger.gz
	SRR6518500.fastq.gz	Fastqsanger.gz
	SRR6518510.fastq.gz	Fastqsanger.gz
	SRR6518481.fastq.gz	Fastqsanger.gz

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Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer

Project description:Increasingly effective therapies targeting the androgen receptor have paradoxically promoted the incidence of neuroendocrine prostate cancer (NEPC), the most lethal subtype of castration-resistant prostate cancer (PCa), for which there is no effective therapy. Here we report that protein kinase C (PKC)l/i is downregulated in de novo and during therapy-induced NEPC, which results in the upregulation of serine biosynthesis through an mTORC1/ATF4-driven pathway. This metabolic reprogramming increases intracellular SAM levels to support cell proliferation and epigenetic changes that favor the development of NEPC characteristics. Altogether, we have uncovered a metabolic vulnerability triggered by PKCl/i deficiency in NEPC, which offers potentially actionable targets to prevent therapy resistance in PCa. This SuperSeries is composed of the SubSeries listed below.

2019-03-05 | GSE109763 | GEO

Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [MicroArray]

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Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [RNA-seq]

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Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [MeDIP-Seq]

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Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer

Project description:Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer

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Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [MicroArray]

Project description:Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [MicroArray]

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Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [MeDIP-Seq]

Project description:Increased Serine and One Carbon Pathway Metabolism by PKCl/i Deficiency Promotes Neuroendocrine Prostate Cancer [MeDIP-Seq]

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Increased Serine and One-Carbon Pathway Metabolism by PKCλ/ι Deficiency Promotes Neuroendocrine Prostate Cancer.

Project description:Increasingly effective therapies targeting the androgen receptor have paradoxically promoted the incidence of neuroendocrine prostate cancer (NEPC), the most lethal subtype of castration-resistant prostate cancer (PCa), for which there is no effective therapy. Here we report that protein kinase C (PKC)λ/ι is downregulated in de novo and during therapy-induced NEPC, which results in the upregulation of serine biosynthesis through an mTORC1/ATF4-driven pathway. This metabolic reprogramming supports cell proliferation and increases intracellular S-adenosyl methionine (SAM) levels to feed epigenetic changes that favor the development of NEPC characteristics. Altogether, we have uncovered a metabolic vulnerability triggered by PKCλ/ι deficiency in NEPC, which offers potentially actionable targets to prevent therapy resistance in PCa.

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PKCl/i inhibition activates an ULK2-mediated interferon response to repress tumorigenesis [ATAC-Seq]

Project description:The interferon (IFN) pathway is critical for cytotoxic T cell activation, which is central to tumor immunosurveillance and successful immunotherapy. We demonstrate here that PKCl/i inactivation results in the hyper-stimulation of the IFN cascade and the enhanced recruitment of CD8+ T cells that impaired the growth of intestinal tumors. PKCl/i directly phosphorylates and represses the activity of ULK2, promoting its degradation through an endosomal microautophagy-driven ubiquitin-dependent mechanism. Loss of PKCl/i results in increased levels of enzymatically active ULK2 that by direct phosphorylation activates TBK1 to foster the activation of the STING-mediated IFN response. PKCl/i inactivation also triggers autophagy that prevents STING degradation by chaperone-mediated autophagy. Thus, PKCl/i is a hub regulating the IFN pathway and three autophagic mechanisms that serve to maintain its homeostatic control. Importantly, single cell multiplex imaging and bioinformatics analysis demonstrated that low PKCl/i levels correlate with enhanced IFN signaling and good prognosis in colorectal cancer patients.

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PKCl/i inhibition activates an ULK2-mediated interferon response to repress tumorigenesis [RNA-Seq]

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