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Effects of ferroptosis inhibition on lung transcriptomics in monocrotaline rats

ABSTRACT: Effects of ferroptosis inhibition on lung transcriptomics in monocrotaline rats

PROVIDER: PRJNA1160920 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30664900_1.fastq.gz	Fastqsanger.gz
	SRR30664900_2.fastq.gz	Fastqsanger.gz
	SRR30664901_1.fastq.gz	Fastqsanger.gz
	SRR30664901_2.fastq.gz	Fastqsanger.gz
	SRR30664902_1.fastq.gz	Fastqsanger.gz

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Effects of ferroptosis inhibition on lung transcriptomics in monocrotaline rats

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Project description:Ferroptosis constitutes a promising therapeutic strategy against cancer by efficiently targeting the highly tumorigenic and treatment-resistant cancer stem cells (CSCs). We previously showed that the lysosomal iron-targeting drug Salinomycin (Sal) was able to eliminate CSCs by triggering ferroptosis. Here, in a well-established breast CSCs model (human mammary epithelial HMLER CD24low/CD44high), we identified that pharmacological inhibition of mechanistic target of rapamycin (mTOR), suppresses Sal-induced ferroptosis. Mechanistically, mTOR inhibition modulates iron cellular flux and prevents the iron and ROS bursts induced by Sal. Besides, integration of multi-omics data identified mitochondria as a key target of Sal action. We demonstrated that mTOR inhibition prevents Sal-induced mitochondrial functional and structural alteration, and that Sal-induced metabolic plasticity is mainly dependent on the mTOR pathway. Overall, our findings provide experimental evidences on the detailed mechanisms of mTOR as a crucial effector of Sal-induced ferroptosis, and gives proof-of-concept that careful evaluation of such combination therapy (here mTOR and ferroptosis co-targeting) is required for effective treatment.

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