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RNA sequencing of HCC cells after endoplasmic reticulum stress induced by tunicamycin

ABSTRACT: RNA sequencing of HCC cells after endoplasmic reticulum stress induced by tunicamycin

PROVIDER: PRJNA859786 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20281587_1.fastq.gz	Fastqsanger.gz
	SRR20281587_2.fastq.gz	Fastqsanger.gz
	SRR20281588_1.fastq.gz	Fastqsanger.gz
	SRR20281588_2.fastq.gz	Fastqsanger.gz
	SRR20281589_1.fastq.gz	Fastqsanger.gz

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Tunicamycin-induced Endoplasmic Reticulum-Quality Control Pathway and Endoplasmic Reticulum-Associated Degradation Mechanism in the diatom Phaeodactylum tricornutum

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RNA sequencing of HCC cells after endoplasmic reticulum stress induced by tunicamycin

Project description:In order to explore the role of ER stress in the development and progression of HCC, RNA sequencing was performed to detect the differential RNA levels before and after ER stress, thus providing strong evidence for the search of ER stress-related genes.

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Tunicamycin-induced Endoplasmic Reticulum-Quality Control Pathway and Endoplasmic Reticulum-Associated Degradation Mechanism in the diatom Phaeodactylum tricornutum

Project description:Tunicamycin inhibits the first step of protein N-glycosylation modification. However, the physiological, transcriptomic, and N-glycomic effects of tunicamycin on important marine diatom Phaeodactylum tricornutum are still unknown. In this study, comprehensive approaches were used to study the effects. The results showed that cell growth and photosynthesis were significantly inhibited in P. tricornutum under the tunicamycin stress. The soluble protein content was significantly decreased, while the soluble sugar and neutral lipid were dramatically increased to orchestrate the balance of carbon and nitrogen metabolism. 0.3 μg m-1 tunicamycin could not complete inhibited the N-glycosylation of protein, but it resulted in the differentially expression of ERQC and ERAD related genes. The upregulation of genes involved in ERQC and the activation of anti-oxidases were speculated to alleviate the tunicamycin stress. The differentially expression of genes related to ERAD was suggested to degrade the unfolded and/or incorrect N-glycoproteins induced by tunicamycin. The identification of mannose-type and complex-type N-glycan structures enriched the N-glycan database of diatom P. tricornutum and provided important information for studying the function of N-glycosylation modification on proteins. All in all, the proposed working models of ERQC and ERAD will provide a solid foundation for further in-depth study the related mechanism and the diatom expression system.

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Chip sequencing after ER stress induced in HCC cells using tunicamycin

Project description:We report the application of the CHIP sequencing-based technology in the high-throughput analysis of histone modifications in HepG2 cells. Endoplasmic reticulum stress related super enhancers were identified and their regulatory target genes were predicted.

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Project description:Hepatocellular carcinoma (HCC) is among the most common cause of cancer-related death worldwide. Previous studies showed that N6-methyladenosine (m⁶A), the most abundant chemical modification in eukaryotic RNAs, is implicated in HCC progression. Using liver-specific conditional knockout mice, here we found that loss of METTL3, the core catalytic subunit of m⁶A methyltransferase, significantly promoted hepatic tumor initiation under various oncogenic challenges, contrary to the previously reported oncogenic role of METTL3 in liver cancer cell lines or xenograft models. Mechanistically, METTL3 deficiency accelerates HCC initiation by inhibiting m6A/Manf/endoplasmic reticulum (ER) stress response. Our findings suggest a tumor-suppressive role for METTL3 in the early stages of HCC, emphasizing the importance of understanding the dynamic role of epigenetic regulation in tumorigenesis and targeted therapy.

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