Similar Datasets
Project description:DEAD-box (DDX) RNA helicases play crucial roles in gene regulation by interacting with RNAs and influencing RNA fate and function. Previously, we have associated DDX24 with vascular development, but its precise role in RNA metabolism remains unclear. In this study, we demonstrate that DDX24 modulated endothelial cell functions by binding to and regulating mRNAs crucial for vascular morphogenesis and angiogenesis. These results establish a link between DDX24-dependent regulation of mRNA stability and endothelial cell function, providing novel therapeutic targets for angiogenesis.
2026-02-20 | GSE256144 | GEO
Project description:DEAD-box (DDX) RNA helicases play crucial roles in gene regulation by interacting with RNAs and influencing RNA fate and function. Previously, we have associated DDX24 with vascular development, but its precise role in RNA metabolism remains unclear. In this study, we demonstrate that DDX24 facilitates the decay of the target mRNAs, in a CCR4-NOT deadenylase complex dependent manner. These results establish a link between DDX24-dependent regulation of mRNA stability and endothelial cell function, providing novel therapeutic targets for angiogenesis.
2026-02-20 | GSE256145 | GEO
Project description:DEAD-box (DDX) RNA helicases play crucial roles in gene regulation by interacting with RNAs and influencing RNA fate and function. Previously, we have associated DDX24 with vascular development, but its precise role in RNA metabolism remains unclear. In this study, we demonstrate that DDX24 modulated endothelial cell functions by binding to and regulating mRNAs crucial for vascular morphogenesis and angiogenesis. We further identify DDX24-bound mRNAs in endothelial cells using crosslinking immunoprecipitation (CLIP) sequencing. Mechanistically, DDX24 facilitates the decay of the target mRNAs, such as CLEC14A and ERG, by recruiting the deadenylase complex CCR4-NOT. These results establish a link between DDX24-dependent regulation of mRNA stability and endothelial cell function, providing novel therapeutic targets for angiogenesis.
2026-02-20 | GSE256143 | GEO
Project description:To investigate the impact of DDX24 mutation on the RNA binding activity in HUVEC cells, we conducted RIP-seq analysis.
2026-02-20 | GSE310774 | GEO
Project description:To investigate the role of DDX24 in vascular smooth muscle cells, RNA-seq of HUASMC/HUVSMC with DDX24 knockdown was performed. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.
2025-05-01 | GSE202486 | GEO
Project description:Accumulating evidence suggests that DEAD-box proteins are essential in RNA metabolism and play pivotal roles in cancer progression. However, the mechanisms underlying how DDX24 drives hepatocellular carcinoma (HCC) remain largely unknown. In this study, we demonstrated that DDX24 was an oncogene and identified RFX8 as a DDX24 promoter-binding protein that transcriptionally upregulated DDX24 expression.
2021-01-29 | PXD022650 | Pride
Project description:Accumulating evidence suggests that DEAD-box proteins are essential in RNA metabolism and play pivotal roles in cancer progression. However, the mechanisms underlying how DDX24 drives hepatocellular carcinoma (HCC) remain largely unknown. In this study, we demonstrated that DDX24 was an oncogene and identified DDX24 promoted HCC development via interacting with NCL.
2021-01-29 | PXD023321 | Pride
Project description:DEAD-box helicase 24 (DDX24) is a member of the DEAD-box protein family, which is essential for various aspects of RNA metabolism. DDX24 has been reported to play a role in ribosome biogenesis, transcription, and mRNA stability. Previous studies have implicated the functions of DDX24 in innate immunity, vascular malformation, cell growth, and cancer progression. Here, we describe a novel function of DDX24 in regulating the oxidative stress response and protecting cells from apoptosis. Our research revealed that DDX24 specifically regulates the expression of the heme oxygenase-1 (HO-1) gene, as determined by RNA sequencing analysis. HO-1 is responsible for degrading heme into carbon monoxide (CO), biliverdin, and ferrous ion (Fe2+), thereby exerting anti-apoptotic and anti-oxidative effects. We validated the regulation of HO-1 by DDX24 in both DDX24-depleted and DDX24-overexpressing HEK293 cells. Our findings indicate that DDX24 is involved in the induction of HO-1 expression under oxidative stress conditions. Importantly, DDX24 regulates the transcription of HO-1 instead of its mRNA stability, likely acting at the promoter and enhancer E1 region of the HO-1 gene. Furthermore, DDX24 depletion in HEK293T cells inhibits cell viability. DDX24 exerts both anti-apoptotic and anti-oxidative effects during oxidative stress. These results suggest that DDX24 plays a crucial role in protecting cells from oxidative stress-induced damage by regulating the transcription of HO-1.
2026-01-01 | GSE299414 | GEO
Project description:Hepatocellular carcinoma (HCC) is not only the fifth most prevalent cancer, presenting a major global health problem, but also among the leading causes of cancer-related deaths worldwide as its therapeutic targets are limited. To identify novel therapeutic targets, elucidate its oncogenic activities and molecular mechanism in HCC is urgent. We used R language edgeR package screened the expression profiles of 374 tissue samples obtained from patients with HCC and 50 samples of normal liver tissues obtained from The Cancer Genome Atlas (TCGA) database. Focusing on DDX24, we explored the functional effect and clinical significance of DDX24 in HCC. We provided evidence that DDX24 was a potential pro-tumorigenic gene in HCC. DDX24 knockdown inhibited HCC cell growth in vitro and in vivo. Mechanistically, RFX8 was proved to be DDX24 promoter-binding protein that transcriptionally upregulated DDX24 expression. Furthermore, we found that DDX24 bound to, and increased the stability of, LAMB1 mRNA by RNA immunoprecipitation (RIP) sequencing and RNA sequencing. Survival analysis indicated that HCC patients with high DDX24, RFX8, or LAMB1 expression exhibited poor prognosis. Our results demonstrated that DDX24 promoted HCC via RFX8/DDX24/LAMB1 pathway, which can be exploited as potential therapeutic target against HCC.
2020-02-21 | GSE145635 | GEO
Project description:Hepatocellular carcinoma (HCC) is not only the fifth most prevalent cancer, presenting a major global health problem, but also among the leading causes of cancer-related deaths worldwide as its therapeutic targets are limited. To identify novel therapeutic targets, elucidate its oncogenic activities and molecular mechanism in HCC is urgent. We used R language edgeR package screened the expression profiles of 374 tissue samples obtained from patients with HCC and 50 samples of normal liver tissues obtained from The Cancer Genome Atlas (TCGA) database. Focusing on DDX24, we explored the functional effect and clinical significance of DDX24 in HCC. We provided evidence that DDX24 was a potential pro-tumorigenic gene in HCC. DDX24 knockdown inhibited HCC cell growth in vitro and in vivo. Mechanistically, RFX8 was proved to be DDX24 promoter-binding protein that transcriptionally upregulated DDX24 expression. Furthermore, we found that DDX24 bound to, and increased the stability of, LAMB1 mRNA by RNA immunoprecipitation (RIP) sequencing and RNA sequencing. Survival analysis indicated that HCC patients with high DDX24, RFX8, or LAMB1 expression exhibited poor prognosis. Our results demonstrated that DDX24 promoted HCC via RFX8/DDX24/LAMB1 pathway, which can be exploited as potential therapeutic target against HCC.
2020-02-21 | GSE145632 | GEO