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RNA-seq of Huh7 cell after G6PD enzyme activity inhibitor RRx-1 treated with 20μM concentrations for 24h

ABSTRACT: RNA-seq of Huh7 cell after G6PD enzyme activity inhibitor RRx-1 treated with 20μM concentrations for 24h

PROVIDER: PRJEB41054 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4781460.fastq.gz	Fastqsanger.gz
	ERR4781461.fastq.gz	Fastqsanger.gz
	ERR4781462.fastq.gz	Fastqsanger.gz
	ERR4781463.fastq.gz	Fastqsanger.gz
	ERR4781458.fastq.gz	Fastqsanger.gz

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RNA-seq of Huh7 cell after G6PD enzyme activity inhibitor RRx-1 treated with 20μM concentrations for 24h

Project description:In order to analyze the changes of G6PD enzyme activity regulating the metabolism and proliferation pathways in HCC cell. After G6PD enzyme activity inhibitor RRx-1 treated with 20μM concentrations for 24h in Huh7 cell. Differential expression of genes were selected after RNA sequencing. Then David Bioinformatics was utilized to identify the most significantly regulated GOTERMs and KEGG pathways based on the transcriptional changes.

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Project description:RNA-seq of Huh7 cell after G6PD enzyme activity inhibitor RRx-1 treated with 20Î¼M concentrations for 24h

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Project description:The spread of cancer to bone is invariably fatal, with complex crosstalk between tumour cells and the bone microenvironment responsible for driving disease progression. By combining in silico analysis of patient datasets with metabolomic profiling of prostate cancer cells cultured with bone cells, we demonstrate the changing energy requirements of prostate cancer cells in the bone microenvironment, identifying the pentose phosphate pathway (PPP) as elevated in prostate cancer bone metastasis, with increased expression of the PPP rate-limiting enzyme (G6PD) associated with a reduction in progression-free survival. Genetic and pharmacologic manipulation demonstrates that G6PD inhibition reduces prostate cancer growth and migration, associated with changes in cellular redox state and increased chemosensitivity. Genetic blockade of G6PD in vivo results in reduction of tumour growth within bone. In summary, we demonstrate the metabolic plasticity of prostate cancer cells in the bone microenvironment, identifying the PPP and G6PD as metabolic targets for the treatment of prostate cancer bone metastasis.

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