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IL-17B/IL-17RB signaling cascade contributes to self-renewal and tumorigenesis of cancer stem cells by regulating Beclin-1 ubiquitination

ABSTRACT: IL-17B/IL-17RB signaling cascade contributes to self-renewal and tumorigenesis of cancer stem cells by regulating Beclin-1 ubiquitination

PROVIDER: PRJNA688691 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13329257_1.fastq.gz	Fastqsanger.gz
	SRR13329257_2.fastq.gz	Fastqsanger.gz
	SRR13329258_1.fastq.gz	Fastqsanger.gz
	SRR13329258_2.fastq.gz	Fastqsanger.gz
	SRR13329259_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

IL-17B/IL-17RB signaling cascade contributes to self-renewal and tumorigenesis of cancer stem cells by regulating Beclin-1 ubiquitination

Project description:Recombinant IL-17B (rIL-17B) promoted the sphere formation ability of CSCs in vitro and enhanced tumor growth and metastasis in vivo. Furthermore, the activation of autophagy was critically involved in IL-17B/IL-17RB-mediated regulation of CSC functions.

2022-01-28 | GSE164038 | GEO

IL-17B/IL-17RB signaling cascade contributes to self-renewal and tumorigenesis of cancer stem cells by regulating Beclin-1 ubiquitination.

Project description:Cancer stem cells (CSCs) are characterized by robust self-renewal and tumorigenesis and are responsible for metastasis, drug resistance, and angiogenesis. However, the molecular mechanisms for the regulation of CSC homeostasis are incompletely understood. This study demonstrated that the interleukin-17 (IL-17)B/IL-17RB signaling cascade promotes the self-renewal and tumorigenesis of CSCs by inducing Beclin-1 ubiquitination. We found that IL-17RB expression was significantly upregulated in spheroid cells and Lgr5-positive cells from the same tumor tissues of patients with gastric cancer (GC), which was closely correlated with the degree of cancer cell differentiation. Recombinant IL-17B (rIL-17B) promoted the sphere-formation ability of CSCs in vitro and enhanced tumor growth and metastasis in vivo. Interestingly, IL-17B induced autophagosome formation and cleavage-mediated transformation of LC3 in CSCs and 293T cells. Furthermore, inhibition of autophagy activation by ATG7 knockdown reversed rIL-17B-induced self-renewal of GC cells. In addition, we showed that IL-17B also promoted K63-mediated ubiquitination of Beclin-1 by mediating the binding of tumor necrosis factor receptor-associated factor 6 to Beclin-1. Silencing IL-17RB expression abrogated the effects of IL-17B on Beclin-1 ubiquitination and autophagy activation in GC cells. Finally, we showed that IL-17B level in the serum of GC patients was positively correlated with IL-17RB expression in GC tissues, and IL-17B could induce IL-17RB expression in GC cells. Overall, the results elucidate the novel functions of IL-17B for CSCs and suggest that the intervention of the IL-17B/IL-17RB signaling pathway may provide new therapeutic targets for the treatment of cancer.

| S-EPMC7994204 | biostudies-literature

IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

Project description:Purpose: Explore IL-17B target genes expression via next-generation sequencing (NGS) in mouse lung tissues. Methods: Overexpress IL-17B in mouse lung tissues via intranasal injection of adenovirus encoding IL-17B (Adv-IL-17B) and empty virus (Adv-EV). Three days after infection lung tisses were removed for RNA collection. Five samples per group were mixed to one sample and used for next RNA purification. RNA samples were then used for high-throughput sequencing according to standard operation based on RNA Hiseq 4000. Results: Using an optimized data analysis workflow, we mapped about 13 million sequence reads per sample to the mouse genome (build mm10) and identified 269 upregulated and 99 downregulated genes in lung after IL-17B overexpression. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.8798. Altered expression of 20 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to lung inflammation and infection. Data analysis with BWA and TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: Our study represents the first detailed analysis of IL-17B induced downstream genes with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. We conclude that RNA-seq based downstream genes characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

2019-02-19 | GSE106380 | GEO

IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

Project description:IL-17B promotes proinflammatory cytokines expression in mouse lung tissues

| PRJNA416508 | ENA

IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (OPC RiboTAG)

Project description:Cerebral small vessel disease and brain white matter injury are worsened by cardiovascular risk factors including obesity. Molecular pathways in cerebral endothelial cells activated by chronic cerebrovascular risk factors alter cell-cell signaling, blocking endogenous and post-ischemic white matter repair. Using cell-specific translating ribosome affinity purification(RiboTag) in white matter endothelia and oligodendrocyte progenitor cells (OPCs), we identify a coordinated interleukin-chemokine signaling cascade within the oligovascular niche of subcortical white matter that is triggered by diet-induced obesity (DIO).DIO induces IL-17B signaling that acts on the cerebral endothelia through IL-17Rb to increase both circulating and local endothelial expression of CXCL5. In white matter endothelia, CXCL5 promotes the association of OPCs with the vasculature and triggers OPC gene expression programs regulating cell migration through chemokine signaling. Targeted blockade of IL-17B reduced vessel-associated OPCs by reducing endothelial CXCL5 expression. In multiple human cohorts, blood levels of CXCL5 function as a diagnostic and prognostic biomarker of vascular cognitive impairment.

2022-11-11 | GSE217354 | GEO

IL-17/CXCL5 signaling within the oligovascular niche mediates human and mouse white matter injury (Tie2-Cre RiboTAG)

2022-11-11 | GSE217355 | GEO

Cutibacterium acnes 17B

Project description:Cutibacterium acnes 17B Genome sequencing and assembly

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Haloplasma contractile SSD-17B

Project description:Haloplasma contractile SSD-17B genome sequencing

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The expression patterns of 17b-estradiol responsive genes in wt MCF7, OHT resistant MCF7 and ICI resistant MCF7

Project description:Compare the expression pattern of 17b-estradiol responsive genes in parent, OHT-resistant and ICI-resistant breast cancer cells. Keywords: 17b-estradiol responsive genes, OHT resistance, Fulvestrand resistance

2007-09-14 | GSE5840 | GEO

Transcription profiling of human wild type MCF7, OHT resistant MCF7 and ICI resistant MCF7 17b-estradiol responsive genes

Project description:Compare the expression pattern of 17b-estradiol responsive genes in parent, OHT-resistant and ICI-resistant breast cancer cells. Experiment Overall Design: Data for 4 replicate experiments performed with biologically independent samples. Experiment Overall Design: KN01M001v0 DMSO (control) wt MCF7 -> GSM136152 Experiment Overall Design: KN01H002v0 DMSO (control) wt MCF7 -> GSM136148 Experiment Overall Design: KN01H003v0 DMSO (control) wt MCF7 -> GSM136150 Experiment Overall Design: KN01H004v0 DMSO (control) wt MCF7 -> GSM136152 Experiment Overall Design: KN01M005v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136153 Experiment Overall Design: KN01H006v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136154 Experiment Overall Design: KN01H007v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136155 Experiment Overall Design: KN01H008v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136156

2008-06-14 | E-GEOD-5840 | biostudies-arrayexpress

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