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Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

ABSTRACT: Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

PROVIDER: PRJNA796277 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17549866.fastq.gz	Fastqsanger.gz
	SRR17549867.fastq.gz	Fastqsanger.gz
	SRR17549868.fastq.gz	Fastqsanger.gz
	SRR17549869.fastq.gz	Fastqsanger.gz
	SRR17549870.fastq.gz	Fastqsanger.gz

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Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

Project description:We have performed a transcriptomics study in which we first apply cisplatin to HeLa cells. Total RNA was isolated from control as well as treated cells and apoptosis was confirmed by Annexin V and 7AAD staining in flow cytometry. Total RNAs were subjected to deep-sequencing to identify differentially expressed mRNAs. We then took advantage of bioinformatic tools to identify which pathways are affected by Cisplatin treatment

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Project description:Cisplatin and similar alkylating chemotherapy agents are the cornerstone treatments for many types of cancers. While effective, these drugs induce long-term side-effects in post-mitotic tissues including the nervous system. There are no known effective pharmacological interventions for chemotherapy-induced neurotoxicities, in part due to our limited understanding of how neurons and other non-dividing cells respond to DNA damage. Here, we show that nucleotide excision repair (NER) is responsible for cisplatin adduct removal in human neurons. However, contrary to its protective role in dividing cells, NER drives neuronal cell death in response to cisplatin. Through DNA repair synthesis, NER exhausts low levels of deoxynucleoside triphosphate (dNTP) pools found in post-mitotic neurons. dNTP pools are first consumed to resolve transcription blocking lesions through transcription-coupled NER. When dNTPs become exhausted, toxic double-strand breaks accumulate across the genome primarily because of incomplete global-genome NER. Supplementation with deoxynucleosides (dN) or genetic upregulation of dNTP production protects neurons from cisplatin-induced cell death. These results identify low levels of endogenous dNTP pools as a vulnerability of post-mitotic cells to DNA damage and suggest nucleoside supplementation as a strategy to protect patients from chemotherapy-induced neurotoxicity.

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