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Positive regulation of oxidative phosphorylation by nuclear myosin 1 protects cells from metabolic reprogramming and tumorigenesis in mice

ABSTRACT: Positive regulation of oxidative phosphorylation by nuclear myosin 1 protects cells from metabolic reprogramming and tumorigenesis in mice

PROVIDER: PRJNA992018 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25180493_1.fastq.gz	Fastqsanger.gz
	SRR25180493_2.fastq.gz	Fastqsanger.gz
	SRR25180494_1.fastq.gz	Fastqsanger.gz
	SRR25180494_2.fastq.gz	Fastqsanger.gz
	SRR25180495_1.fastq.gz	Fastqsanger.gz

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Positive regulation of oxidative phosphorylation by nuclear myosin 1 protects cells from metabolic reprogramming and tumorigenesis in mice

Project description:Metabolic reprograming is one of the hallmarks of tumorigenesis. Using a combination of multi-omics, here we show that nuclear myosin 1 (NM1) serves a key regulator of cellular metabolism. As part of nutrient-sensing PI3K/Akt/mTOR pathway, NM1 forms a positive feedback loop with mTOR, and directly affects mitochondrial oxidative phosphorylation via transcriptional regulation of mitochondrial transcription factors TFAM and PGC1α. NM1 depletion leads to a suppression of PI3K/Akt/mTOR pathway, underdevelopment of mitochondria inner cristae and redistribution of mitochondria within a cell, which is associated with reduced expression of oxidative phosphorylation genes, decreased mitochondrial DNA copy number, and deregulated mitochondrial dynamics. This leads to a metabolic reprogramming of NM1 KO cells from oxidative phosphorylation to aerobic glycolysis and with that associated metabolomic profile typical for cancer cells, namely, increased amino acid-, fatty acid-, and sugar metabolism, and increase in glucose uptake, lactate production and intracellular acidity. We show that NM1 KO cells are able to form solid tumors in a nude mouse model even though they have supressed PI3K/Akt/mTOR signalling pathway suggesting that the metabolic switch towards aerobic glycolysis provide a sufficient signal for carcinogenesis. We suggest that NM1 plays a key role as tumor suppressor and that NM1 depletion may be partly responsible for the Warburg effect at the early onset of tumorigenesis.

2023-07-13 | GSE236679 | GEO

Nuclear Myosin 1 depletion leads to a metabolic reprogramming of cells and tumorigenesis in mice

2022-06-27 | GSE206858 | GEO

IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia

Project description:IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia

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Oxidative phosphorylation promotes primary melanoma invasion

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IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia [snRNA-Seq]

Project description:IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia [snRNA-Seq]

| PRJNA1190429 | ENA

Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis

Project description:Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis

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Positive regulation of oxidative phosphorylation by nuclear myosin 1 protects cells from metabolic reprogramming and tumorigenesis in mice.

Project description:Metabolic reprogramming is one of the hallmarks of tumorigenesis. Here, we show that nuclear myosin 1 (NM1) serves as a key regulator of cellular metabolism. NM1 directly affects mitochondrial oxidative phosphorylation (OXPHOS) by regulating mitochondrial transcription factors TFAM and PGC1α, and its deletion leads to underdeveloped mitochondria inner cristae and mitochondrial redistribution within the cell. These changes are associated with reduced OXPHOS gene expression, decreased mitochondrial DNA copy number, and deregulated mitochondrial dynamics, which lead to metabolic reprogramming of NM1 KO cells from OXPHOS to aerobic glycolysis.This, in turn, is associated with a metabolomic profile typical for cancer cells, namely increased amino acid-, fatty acid-, and sugar metabolism, and increased glucose uptake, lactate production, and intracellular acidity. NM1 KO cells form solid tumors in a mouse model, suggesting that the metabolic switch towards aerobic glycolysis provides a sufficient carcinogenic signal. We suggest that NM1 plays a role as a tumor suppressor and that NM1 depletion may contribute to the Warburg effect at the onset of tumorigenesis.

| S-EPMC10564744 | biostudies-literature

IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia [bulk RNA-Seq]

Project description:IL-1 protects from fatal systemic candidiasis by inhibition of oxidative phosphorylation and hypoxia [bulk RNA-Seq]

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PRMT1 methylation of WTAP promotes multiple myeloma tumorigenesis by activating oxidative phosphorylation via m6A modification of NDUFS6

Project description:PRMT1 methylation of WTAP promotes multiple myeloma tumorigenesis by activating oxidative phosphorylation via m6A modification of NDUFS6

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eIF4E phosphorylation promotes tumorigenesis and is associated with prostate cancer progression

Project description:Translational regulation plays a critical role in cell growth and proliferation, and its dysregulation results in cancer. Aberrant expression of the mRNA 5’cap-binding protein, eIF4E, has been implicated in cancer development and progression. eIF4E activity is promoted by phosphorylation. Here we show that “knock-in” mice in which eIF4E cannot be phosphorylated are resistant to tumorigenesis in a prostate cancer model. We identify multiple candidate genes involved in the resistance to oncogenic transformation. Importantly, phosphorylation of eIF4E is increased in hormone-refractory prostate cancer, the deadliest stage of the disease. Our results highlight eIF4E phosphorylation as a critical event in tumorigenesis. Comaparison of total RNA and polysomal RNA from mouse embryo fibroblasts derived from WT and eIF4E-KI (non phosphorylatable eIF4E) mice

2010-08-17 | E-GEOD-17451 | biostudies-arrayexpress

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