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DGAT1 is a bona fide oncogene stimulating cell growth and suppressing oxidative stress while enabling fatty acid accumulation

ABSTRACT: DGAT1 is a bona fide oncogene stimulating cell growth and suppressing oxidative stress while enabling fatty acid accumulation

PROVIDER: PRJNA604017 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10990701_1.fastq.gz	Fastqsanger.gz
	SRR10990701_2.fastq.gz	Fastqsanger.gz
	SRR10990702_1.fastq.gz	Fastqsanger.gz
	SRR10990702_2.fastq.gz	Fastqsanger.gz
	SRR10990703_1.fastq.gz	Fastqsanger.gz

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DGAT1 phosphoproteome and long-term proteome

Project description:Enhanced fatty acid (FA) synthesis and uptake underpin the sustained membrane biogenesis and ATP production required for melanoma cell growth and division1-4. However, to thrive, melanoma cells must avoid a potential reduction in cell growth signalling, rampant reactive oxygen species (ROS) generation, and the build-up of toxic lipid species that can accompany excess free FA5. Here, we uncover and address the significance of frequent amplification and up-regulation of the Diacylglycerol O-acyltransferase 1 (DGAT1) gene in melanoma, whose encoded product catalyses the final step of Triacyglyceride (TAG) synthesis. Consistent with the classification of DGAT1 as an oncogene, we found that forced DGAT1 expression in p53 mutant zebrafish melanocytes was sufficient to induce melanoma, and accelerated melanoma progression initiated by co-expression of oncogenic BRAF or NRAS. Regarding DGAT1 function in human melanoma cells, its depletion, or alternatively pharmacological inhibition, suppressed mTOR-S6K signalling and increased levels of acyl carnitine species— FA derivatives that are the limiting substrate for FA oxidation (FAO). In turn, increased FAO induced mitochondrial malfunction, ROS generation, and lipid peroxidation. However, the resultant oxidative stress induced NRF2 and SESTRIN2 (SESN2) expression, which limited the extent of cell death. Conversely, DGAT1 over-expression enhanced mTOR-S6K signalling and cell growth, and protected against ROS, particularly in hypoxic conditions. Together, our data establish DGAT1 as a bona fide oncogene essential in melanoma cells for enabling FA accumulation.

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DGAT1 is a bona fide oncogene stimulating cell growth and suppressing oxidative stress while enabling fatty acid accumulation

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