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ABSTRACT: HEI-OC1 cells sequencing

PROVIDER: PRJNA1080024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28083319_1.fastq.gz	Fastqsanger.gz
	SRR28083319_2.fastq.gz	Fastqsanger.gz
	SRR28083320_1.fastq.gz	Fastqsanger.gz
	SRR28083320_2.fastq.gz	Fastqsanger.gz
	SRR28083321_1.fastq.gz	Fastqsanger.gz

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Project description:Cisplatin, a utilized anticancer drug in clinical practice, induces sensorineural hearing loss (SNHL) in patients. However, the precise mechanism underlying cisplatin-associated ototoxicity remains unknown. HEI-OC1 cells are immortalized cells derived from the organs of Corti mice and nuclear factor erythroid 2-related factor 2 （Nrf2） knockout (KO) significantly enhances cisplatin resistance in these cells. The exploration of transcriptomic data from Nrf2 KO has significant implications for the identification of novel targets to enhance HEI-OC1 cisplatin resistance in Nrf2 KO and for understanding the biological characteristics associated with SNHL. The RNA-seq analysis revealed a significant enrichment of differentially expressed genes (DEGs) in the Nrf2 KO model within key signaling pathways, including the PI3K-Akt, MAPK, as well as Glutathione metabolism signaling pathways. Notably, expression levels of 17 specific genes were confirmed by RT-qPCR (Real-time Quantitative-PCR). The biomarkers identified in this study may be key to understanding the biological mechanism by which Nrf2 KO strongly increases HEI-OC1 cisplatin resistance, and by targeting the PI3K-Akt, MAPK, Glutathione metabolism signaling pathways provide new ideas for the prevention and treatment of cisplatin-induced SNHL.

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