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Creatine mediated crosstalk between adipocytes and cancer cells regulates obesity-driven breast cancer

ABSTRACT: Creatine mediated crosstalk between adipocytes and cancer cells regulates obesity-driven breast cancer

PROVIDER: PRJNA693853 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13499424.fastq.gz	Fastqsanger.gz
	SRR13499425.fastq.gz	Fastqsanger.gz
	SRR13499426.fastq.gz	Fastqsanger.gz
	SRR13499427.fastq.gz	Fastqsanger.gz
	SRR13499428.fastq.gz	Fastqsanger.gz

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Creatine mediated crosstalk between adipocytes and cancer cells regulates obesity-driven breast cancer

Project description:Obesity is a major risk factor for adverse outcomes in breast cancer. Maguire, Ackerman et al. reveal Gatm and Acsbg1 as molecular regulators of obesity-driven breast cancer progression. They further show that in obesity creatine is a key metabolite in the crosstalk between adipocytes and breast tumors.

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Increased phosphocreatine/creatine ratio in white adipocytes promotes inflammation

Project description:The mechanisms promoting disturbed white adipocyte function in obesity remain largely unclear. Herein, we integrate white adipose tissue (WAT) metabolomic and transcriptomic data from clinical cohorts and find that the WAT phosphocreatine/creatine ratio is increased and creatine kinase-B expression and activity is decreased in the obese state. . In human in vitro and murine in vivo models, we demonstrate that decreased phosphocreatine metabolism in white adipocytes alters AMPK activity via effects on ATP/ADP levels, independently of WAT beigeing. This disturbance promotes a pro-inflammatory profile characterized, in part, by increased CCL2 production. These data suggest that the phosphocreatine/creatine system links cellular energy shuttling with pro-inflammatory responses in human and murine white adipocytes. Our findings provide unexpected perspectives on the mechanisms driving WAT inflammation in obesity and may present avenues to target adipocyte dysfunction.

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Creatine-mediated crosstalk between adipocytes and cancer cells regulates obesity-driven breast cancer.

Project description:Obesity is a major risk factor for adverse outcomes in breast cancer; however, the underlying molecular mechanisms have not been elucidated. To investigate the role of crosstalk between mammary adipocytes and neoplastic cells in the tumor microenvironment (TME), we performed transcriptomic analysis of cancer cells and adjacent adipose tissue in a murine model of obesity-accelerated breast cancer and identified glycine amidinotransferase (Gatm) in adipocytes and Acsbg1 in cancer cells as required for obesity-driven tumor progression. Gatm is the rate-limiting enzyme in creatine biosynthesis, and deletion in adipocytes attenuated obesity-driven tumor growth. Similarly, genetic inhibition of creatine import into cancer cells reduced tumor growth in obesity. In parallel, breast cancer cells in obese animals upregulated the fatty acyl-CoA synthetase Acsbg1 to promote creatine-dependent tumor progression. These findings reveal key nodes in the crosstalk between adipocytes and cancer cells in the TME necessary for obesity-driven breast cancer progression.

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Increased phosphocreatine/creatine ratio in white adipocytes promotes inflammation

Project description:Increased phosphocreatine/creatine ratio in white adipocytes promotes inflammation

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Gene-chip studies of adipogenesis-regulated microRNAs in mouse primary adipocytes and human obesity

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