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HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop

ABSTRACT: HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop

PROVIDER: PRJNA665516 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12708067_1.fastq.gz	Fastqsanger.gz
	SRR12708067_2.fastq.gz	Fastqsanger.gz
	SRR12708068_1.fastq.gz	Fastqsanger.gz
	SRR12708068_2.fastq.gz	Fastqsanger.gz
	SRR12708069_1.fastq.gz	Fastqsanger.gz

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HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [miRNA-seq]

Project description:Hypoxia has crucial functions in cervical cancer development and metastasis by inducing the level of numerous genes, including microRNA genes. But we know little about how the hypoxia factors and microRNAs orchestrate to regulate hallmarks of cervical cancer cells. Here, we show that hypoxia-induced overexpression HIF-3α increased the expression of dozens of miRNAs, including miR-630. Stable overexpression of miR-630 in HeLa cells promotes cancer hallmarks, including radioresistance, inhibition of apoptosis, increased migration and invasion, and EMT-mediated metastasis. Stable inhibition of miR-630 showed opposite features. Further experiment showed the activation of miR-630 was induced by hypoxia treatment. For the molecular mechanism, we used RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing experiments (ChIP-seq) to investigate the targets of HIF-3α. We showed that hypoxia induces expression of HIF-3α to activate miR-630 expression by directly binding to its promoter. Meanwhile, miR-630 positively regulates HIF-1α expression, but represses HIF-1α. Taken together, our findings implicate a novel hypoxia-induced HIF3a-miR-630 regulatory feedback loop contributing to metastasis and progression of cervical cancer cells, and suggest HIF3a and miR630 might be applied as a potential biomarker and therapeutic target for cervical cancer.

2023-09-24 | GSE158531 | GEO

HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [RNA-seq]

2023-09-24 | GSE158530 | GEO

HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [ChIP-seq]

2023-09-24 | GSE158529 | GEO

HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [ChIP-seq]

Project description:HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [ChIP-seq]

| PRJNA665517 | ENA

HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [RNA-seq]

Project description:HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [RNA-seq]

| PRJNA665518 | ENA

HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [miRNA-seq]

Project description:HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop [miRNA-seq]

| PRJNA665519 | ENA

HIF-3α-induced miR-630 expression promotes cancer hallmarks in cervical cancer cells by forming a positive feedback loop

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

2023-09-24 | GSE158532 | GEO

HIF-3<i>α</i>-Induced miR-630 Expression Promotes Cancer Hallmarks in Cervical Cancer Cells by Forming a Positive Feedback Loop.

Project description:PurposeHypoxia has crucial functions in the development and metastasis of cervical cancer by inducing the expression of numerous genes, including microRNA genes. But we know little about how the hypoxia factors and microRNAs orchestrate to regulate hallmarks of cervical cancer cells.MethodsWe conducted RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) experiments to investigate the targets of HIF-3α or miR-630. ChIP-qPCR and RT-qPCR were carried out to validate the results of ChIP-seq and RNA-seq. Cellular, molecular, and radiation experiments were conducted to explore the functions of miR-630.ResultsIn this study, we showed that hypoxia-induced overexpression of HIF-3α increased the expression of dozens of miRNAs, including miR-630. Hypoxia could also directly induce miR-630 expression. ChIP-seq data showed that HIF-3α activates miR-630 expression by directly binding to the promoter of its host gene. Meanwhile, stable overexpression of miR-630 increased the expression of HIF-3α, but repressed the expression of HIF-1α, indicating a positive feedback loop between HIF-3α and miR-630. Consequently, stable overexpression of miR-630 in HeLa cells promotes cancer hallmarks, including radioresistance, inhibition of apoptosis, increased migration and invasion, and EMT-mediated metastasis. Meanwhile, inhibition of miR-630 showed opposite features.ConclusionTaken together, our findings indicate a novel hypoxia-induced HIF-3α and miR-630 regulatory feedback loop contributing to metastasis and progression of cervical cancer cells and suggest that HIF-3α and miR-630 might act as potential biomarkers and therapeutic targets for cervical cancer in the future.

| S-EPMC9584697 | biostudies-literature

GETomics based bulk-RNA sequencing revealed HIF-3α prevents COPD by inhibiting alveolar epithelial cell ferroptosis via the HIF-3α-GPx4 axis.

Project description:COPD patients are largely asymptomatic until later stages when prognosis is generally poor. Here, by shifting the focus forward to pre-COPD and smoking stages, we found the peak of reactive oxygen species (ROS) level and hypoxia character are enriched in pre-COPD samples, and hypoxia inducible factor (HIF)-3α is the key factor. Smoking induced regional tissue hypoxia and emphysema have been found in COPD patients. However, the mechanisms underlying hypoxia especially HIF-3α and COPD have not been investigated. In this study, by leveraging scRNA-seq and EpCAM co-localization analysis we identified HIF-3α is downregulated in alveolar epithelial cells in COPD. In vitro experiments using lentivirus transfection, bulk-RNA seq and RSL3 we found the activation of HIF-3α-GPx4 axis inhibits alveolar epithelial cell ferroptosis under the treatment of cigarettes smoking extracts (CSE). Further results from SftpcCreert2/+R26LSL-Hif3a knock-in mice demonstrated overexpression of HIF-3α inhibits alveolar epithelial cells ferroptosis and prevents the declining of lung function. Our data suggest the activation of HIF-3α-GPx4 axis prevents COPD by inhibiting alveolar epithelial cells ferroptosis. By leveraging this comprehensive analysis method, more promising treatment targets will be found and enhance our understanding to the pathogenesis.

2024-10-09 | GSE275503 | GEO

Clostridioides difficile 630

Project description:Clostridioides difficile 630 Genome sequencing

| PRJNA354635 | ENA