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

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

PROVIDER: PRJNA853056 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19854954_1.fastq.gz	Fastqsanger.gz
	SRR19854954_2.fastq.gz	Fastqsanger.gz
	SRR19854955_1.fastq.gz	Fastqsanger.gz
	SRR19854955_2.fastq.gz	Fastqsanger.gz
	SRR19854956_1.fastq.gz	Fastqsanger.gz

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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.

2023-01-15 | GSE206962 | GEO

Transcriptional regulation of Th17 differentiation by mitochondrial oxidative phosphorylation

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Oxidative phosphorylation promotes primary melanoma invasion

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Oxidative phosphorylation selectively orchestrates tissue macrophage homeostasis

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CAV2-expressing Nerves induce Metabolic Switch toward Mitochondrial Oxidative Phosphorylation to Promote Cancer Stemness

Project description:CAV2-expressing Nerves induce Metabolic Switch toward Mitochondrial Oxidative Phosphorylation to Promote Cancer Stemness

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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

circZFR promote lung carcinogenesis and oxidative phosphorylation by modulating alternative splicing

Project description:circZFR promote lung carcinogenesis and oxidative phosphorylation by modulating alternative splicing

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CAV2-expressing Nerves induce Metabolic Switch toward Mitochondrial Oxidative Phosphorylation to Promote Cancer Stemness

Project description:Cancer cells and the nervous system engage in a dynamic interplay, significantly influencing initiation and progression in head and neck squamous cell carcinoma (HNSCC). Our findings highlight that cancer cells drive an increase in caveolin-2 (Cav2) expression within trigeminal ganglia and associated neural fibers in the tumor milieu, fostering a reciprocal attractant relationship between tumor cells and nerves. Notably, the knockout of Cav2, either globally or specifically in sensory neurons or glial cells, markedly attenuates the growth of orthotopically implanted tongue tumors. Moreover, Cav2-expressing nerves are implicated in shifting cancer cell metabolism towards mitochondrial oxidative phosphorylation, a process involved in maintenance of cancer stem cells (CSCs). Our results also demonstrate that Cav2-expressing nerves confer stemness properties to cancer cells. Disruption of Cav2 expression, both globally and in specific neural cell types, impedes tumorigenesis and progression in a 4-NQO- induced HNSCC mouse model.This interplay observed between cancer cells, neurons, and glial cells suggests a potential mechanism through which tumor-associated nerves might influence cancer stemness via metabolic reprogramming. This highlights a possible new direction for anticancer therapy that warrants further investigation.

2025-02-04 | GSE288675 | GEO

Transcription profiling of human fibroblast RNA from patient with a mitochondrial oxidative phosphorylation complex I deficency vs normal fibroblast RNA

Project description:Comparison of fibroblast RNA from patient with a mitochondrial oxidative phosphorylation complex I deficency to normal fibroblast RNA.<br><br>Note: this experiment submission is not fully MIAME compliant, due to the unavailability of oligonucleotide sequences on the A-MEXP-70 array ("Adelaide, H.sapiens, 19k array, version 1").

2004-09-01 | E-MEXP-118 | biostudies-arrayexpress

Transcription profiling of human fibroblast RNA from a patient with a mitochondrial oxidative phosphorylation complex I deficiency vs normal fibroblast RNA

Project description:Comparison of fibroblast RNA from a patient with a mitochondrial oxidative phosphorylation comnplex I deficiency against normal fibroblast RNA.<br><br>Note: this experiment submission is not fully MIAME compliant, due to the unavailability of oligonucleotide sequences on the A-MEXP-70 array ("Adelaide, H.sapiens, 19k array, version 1").

2004-09-01 | E-MEXP-119 | biostudies-arrayexpress

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