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Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia based on RNA sequencing

ABSTRACT: Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia based on RNA sequencing

PROVIDER: PRJNA771566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16352900_1.fastq.gz	Fastqsanger.gz
	SRR16352900_2.fastq.gz	Fastqsanger.gz
	SRR16352901_1.fastq.gz	Fastqsanger.gz
	SRR16352901_2.fastq.gz	Fastqsanger.gz
	SRR16352902_1.fastq.gz	Fastqsanger.gz

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Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia

Project description:Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia

| PRJNA771563 | ENA

Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia based on miRNA sequencing

Project description:We established cell models of hypoxia, and the number of autophagic vacuoles was observed by electron microscopy. Autophagy associated proteins and invasion were evaluated. RNA sequencing was used to identify DEmRNAs and DEmiRNAs to study the mechanism of hypoxia-induced autophagy in liver cancer cells. Results: We found that hypoxia might promote liver cancer cell invasion by inducing autophagy. In addition, a total of 407 shared DEmRNAs and 57 shared DEmiRNAs were identified in both HCCLM3 autophagy group and SMMC-7721 autophagy group compared with normal controls. Furthermore, 278 DEmRNAs were identified cancer autophagy-specific DEmRNAs and 24 DEmiRNAs were identified cancer autophagy-specific DEmRNA and DEmiRNAs. Finally, we obtained 19 DEmiRNAs with high degree based on the DEmiRNA-DEmRNA interaction network. Among them, hsa-miR-483-5p, hsa-miR-4739, has-miR-214-3p and has-miR-296-5p may be potential gene signatures related to liver cancer autophagy.

2022-05-25 | GSE185853 | GEO

Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia based on RNA sequencing

2022-05-25 | GSE185969 | GEO

Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia based on miRNA sequencing

Project description:Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia based on miRNA sequencing

| PRJNA771003 | ENA

Exploring the underlying mechanism of autophagy in liver cancer cells under hypoxia

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-25 | GSE185971 | GEO

Autophagy regulated by the HIF/REDD1/mTORC1 signaling is progressively increased during erythroid differentiation under hypoxia

Project description:For hematopoietic stem and progenitor cells (HSPCs), hypoxia is a specific microenvironment known as the hypoxic niche. The role of hypoxia in maintaining quiescence, self-renewal and proliferation of HSPCs has been more elaborated. What remains unclear is the regulation of hypoxia on HSPC differentiation, especially on the differentiation of HSPCs into erythrocytes. In this study, we show that hypoxia evidently accelerates erythroid differentiation, and in this process effectively enhances autophagy which rapidly supplies cellular components through degradation of organelles or proteins to meet the needs of cell stress or development. In order to ascertain whether autophagy mediates the erythroid differentiation promoted by hypoxia, we analyze the perturbation of erythroid differentiation after pharmacological and genetic interference with autophagy, and address that autophagy is required for hypoxia-accelerated erythroid differentiation. Transcriptomics reveals HIF-1 and mTORC1 pathways may function as the upstream of autophagy to regulate erythroid differentiation under hypoxia. We further determine that mTORC1 signaling is suppressed by hypoxia to relieve its inhibition of autophagy. In addition, we also discover a new regulatory pattern that with the process of erythroid differentiation, mTORC1 activity gradually decreases and autophagy activity increases concomitantly. Moreover, we provide evidence that HIF-1 target gene REDD1, which inhibits mTORC1 activity, is dramatically upregulated under hypoxia. Silencing REDD1 expression activates mTORC1 signaling and impairs the enhanced autophagy and the accelerated erythroid differentiation under hypoxia. Together, our study reveals that hypoxia is conductive to accelerating erythroid differentiation, in which autophagy induced by the HIF-1/REDD1/mTORC1 pathway plays a pivotal role.

2022-04-04 | GSE199778 | GEO

Autophagy is essential for tumor development and survival in hypoxia and in vivo in glioblastoma. (Provisional)

Project description:Hypoxia is negatively associated with glioblastoma patient survival and contributes strongly to tumor resistance. Unfortunately novel anti-angiogenic therapy increases hypoxia and activates survival pathways in tumor cells leading to inevitable tumor relapse. Here we demonstrate that primary glioma cultures and cell lines depend on autophagy to survive severe hypoxia but also at normal oxygen levels. Positive regulators of autophagy are expressed at higher levels in tumor cells and induction in severe hypoxia is more prominent compared to normal brain cells. We demonstrate that autophagy is an essential/critical target for novel treatment in glioblastoma. We show ATG9A is induced by severe hypoxia and could be a novel player of the autophagic response in glioma cells. ATG9A targeting inhibited tumor growth, suggesting an essential role in glioma cell survival in vivo. While autophagy induction was also observed in normal astrocytes, glioma cells displayed a higher sensitivity towards autophagy inhibitors. Importantly, patient-derived cultures exhibited varying sensitivity towards anti-autophagy treatment, where certain cultures were dependent on autophagy already in normoxic conditions. The treatment of tumor bearing mice with the autophagy inhibitor chloroquine significantly increased mice survival, but combination treatment of the agent with bevacizumab did not reveal additive or synergistic effect. The present study demonstrates that inhibition of autophagy using chloroquine as a single agent provides a novel treatment strategy against glioblastoma. It remains to be seen whether autophagy inhibition will improve current standard of care treatment of newly diagnosed glioblastoma patients and whether more specific inhibitors will lead to stronger therapeutic outcome. (Provisional)

2015-11-10 | E-MTAB-3085 | biostudies-arrayexpress

Oxygen-sensitive methylation of ULK1 is required for hypoxia-induced autophagy

Project description:Hypoxia is a physiological stress that frequently occurs in solid tissues. Autophagy, a ubiquitous degradation/recycling system in eukaryotic cells, renders cells tolerant to multiple stressors. However, the mechanisms underlying autophagy initiation upon hypoxia remains unclear. This study identifies an oxygen-sensitive methylation of ULK1 with an important role in hypoxic stress adaptation by promoting autophagy induction.

2022-01-25 | PXD031209 |

C28 induced autophagy and the underlying mechanism of female germline stem cells in vitro

Project description:We use RNA-seq and ChIP-seq to explore the underlying mechanism of 028-induced autophagy in female germline stem cells in vitro

2022-08-23 | GSE136386 | GEO

Exploring the underlying molecular mechanism of liver cancer cells under hypoxia based on RNA sequencing.

Project description:BackgroundThe aim of our study was to use the differentially expressed mRNAs (DEmRNAs) and differentially expressed miRNAs (DEmiRNAs) to illustrate the underlying mechanism of hypoxia in liver cancer.MethodsIn this study, a cell model of hypoxia was established, and autophagy activity was measured with western blotting and transmission electron microscopy. The effect of hypoxia conditions on the invasion of liver cancer cell was evaluated. RNA sequencing was used to identify DEmRNAs and DEmiRNAs to explore the mechanism of hypoxia in liver cancer cells.ResultsWe found that autophagy activation was triggered by hypoxia stress and hypoxia might promote liver cancer cell invasion. In addition, a total of 407 shared DEmRNAs and 57 shared DEmiRNAs were identified in both HCCLM3 hypoxia group and SMMC-7721 hypoxia group compared with control group. Furthermore, 278 DEmRNAs and 24 DEmiRNAs were identified as cancer hypoxia-specific DEmRNAs and DEmiRNAs. Finally, we obtained 19 DEmiRNAs with high degree based on the DEmiRNA-DEmRNA interaction network. Among them, hsa-miR-483-5p, hsa-miR-4739, hsa-miR-214-3p and hsa-miR-296-5p may be potential gene signatures related to liver cancer hypoxia.ConclusionsOur study may help to understand the potential molecular mechanism of hypoxia in liver cancer.

| S-EPMC9121577 | biostudies-literature

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