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Mitochondrial oxidative transport is inhibited by NDUFA4L2 to promote primary tumor escape [ATAC-Seq]

ABSTRACT: Mitochondrial oxidative transport is inhibited by NDUFA4L2 to promote primary tumor escape [ATAC-Seq]

PROVIDER: PRJNA1260555 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33476426_1.fastq.gz	Fastqsanger.gz
	SRR33476426_2.fastq.gz	Fastqsanger.gz
	SRR33476427_1.fastq.gz	Fastqsanger.gz
	SRR33476427_2.fastq.gz	Fastqsanger.gz
	SRR33476428_1.fastq.gz	Fastqsanger.gz

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Mitochondrial oxidative transport is inhibited by NDUFA4L2 to promote primary tumor escape [RNA-Seq]

Project description:Mitochondrial oxidative transport is inhibited by NDUFA4L2 to promote primary tumor escape [RNA-Seq]

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Mitochondrial oxidative transport is inhibited by NDUFA4L2 to promote primary tumor escape [RNA-Seq]

Project description:Metastases cause most cancer deaths and reflect cellular transitions from epithelial to mesenchymal states (EMT) that enable primary tumor escape to seeding and growth at metastatic sites. Rare cancer-driving mutations that disrupt mitochondrial oxidative metabolism (OxPhos) can promote EMT, yet molecular mechanisms that more broadly link metabolism to metastases are uncertain. Analyses of clear cell renal cell carcinoma (RCC) cells identified the hypoxia-induced mitochondrial electron transport inhibitor, NDUFA4L2, as highly enriched in cancer cells with EMT signatures. NDUFA4L2 suppressed OxPhos, altering levels of metabolites that govern chromatin accessibility of EMT-related loci. NDUFA4L2 specifically promoted cell escape from primary orthotopic RCC rather than colonization to drive lung metastasis. These results demonstrate OxPhos inhibition by NDUFA4L2 is essential for RCC cells undergoing EMT to escape primary tumors.

2025-05-12 | GSE296702 | GEO

Mitochondrial oxidative transport is inhibited by NDUFA4L2 to promote primary tumor escape [ATAC-Seq]

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Transcriptional regulation of Th17 differentiation by mitochondrial oxidative phosphorylation

Project description:We found that mitochondrial oxidative phosphorylation (OXPHOS) plays a critical role in Th17 lineage specification. CD4 T cells differentiated under OXPHOS inhibited conditions show altered metabolic gene profiles (mitochondrial function, glycolysis, and TCA cycle) and pathways associated with cell proliferation. Furthermore, gene set enrichment analysis (GSEA) revealed that mitochondrial respiration impacts transcriptional profiles related to Th17 pathogenic signatures and BATF-sensitive gene clusters. Our study reveals a regulatory role of mitochondrial OXPHOS in transcriptional programming of Th17 lineage commitment.

2020-01-28 | GSE115282 | GEO

Colon cancer cells after escape of late apoptosis [exp_1]

Project description:In order to explore the potential role of escape of late apoptosis in metastasis, we induced apoptosis and subsequently inhibited the death process in a primary culture of colon cancer cells. Here we wanted to explore the transcriptome of such "undead" cells 7 days after apoptosis induction.

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Mitochondrial fatty acid synthesis coordinates mitochondrial oxidative metabolism

Project description:Mitochondrial fatty acid synthesis coordinates mitochondrial oxidative metabolism

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Escape from X inactivation in mouse tissues (RNA-Seq)

Project description:X chromosome inactivation (XCI) silences most genes on one X chromosome in female mammals, but some genes escape XCI. To identify escape gene in vivo and to explore molecular mechanisms that regulate this process we analyzed the allele-specific expression and chromatin structure of X-linked genes in mouse tissues and cells with skewed XCI and distinguishable alleles based on single nucleotide polymorphisms. Using a new method to estimate allelic expression, we demonstrate a continuum between complete silencing and significant expression from the inactive X (Xi). Few genes (2-3%) escape XCI to a significant level and only a minority differs between mouse tissues, suggesting stringent silencing and escape controls. Allelic profiles of DNase I hypersensitivity and RNA polymerase II occupancy of genes on the Xi correlate with escape from XCI. Allelic binding profiles of the DNA binding protein CCCTC-binding factor (CTCF) in different cell types indicate that CTCF binding at the promoter correlates with escape. Importantly, CTCF binding at the boundary between escape and silenced domains may prevent the spreading of active escape chromatin into silenced domains. Examination of allelic expression in mouse hybrid tissues.

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Escape from X inactivation in mouse tissues (ChIP-Seq)

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Mitochondrial reverse electron transport in myeloid cells perpetuates neuroinflammation

Project description:Sustained smouldering, or low grade, activation of myeloid cells is a common hallmark of several chronic neurological diseases, including multiple sclerosis. Distinct metabolic and mitochondrial features of myeloid cells guide diverse functional states. How these features act to perpetuate neuroinflammation is currently unknown. Using a multiomics approach, we identify a new molecular signature that perpetuates the activation of microglia by the reverse electron transport through complex I and the subsequent production of reactive oxygen species. Blocking reverse electron transport in pro-inflammatory myeloid cells protects against neurotoxic damage and improves functional outcomes in animal disease models in vivo. Our data show that reverse electron transport in myeloid cells is a potential new therapeutic target to foster neuroprotection in smouldering inflammatory central nervous system diseases.

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Antiandrogen treatment induces mitochondrial oxidative phosphorylation to promote castration resistance in prostate cancer

Project description:Tumor recurrence and therapy resistance are generally accompanied by alterations in cellular metabolism. However, the mechanism by which metabolic conversion occurs and contributes to castration-resistant prostate cancer (CRPC) remains unclear. Here, we demonstrate that androgen receptor signaling inhibitors (ARSI)-induced mitochondrial oxidative phosphorylation (OXPHOS) is critical for CRPC development. Our findings indicate that prostate cancer cells exhibit increased mitochondrial OXPHOS following ARSI treatment; however, there is no significant change in glycolytic activity. Importantly, this metabolic conversion relies on increased glucose and glutamine utilization. Mechanistically, ARSI treatment induces oxidative stress, resulting in AMPK/PGC-1α-dependent metabolic conversion. High mitochondrial OXPHOS in turn renders prostate cancer cells resistant to ARSI. Pharmacological inhibition of mitochondrial OXPHOS shows promising treatment efficacy for CRPC and synergizes with ARSI to inhibit CRPC growth. Collectively, we demonstrate the metabolic plasticity of prostate cancer cells following ARSI treatment, identifying mitochondrial OXPHOS as a metabolic target for CRPC treatment.

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