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Last update 08 May 2025

DDX24

Last update 08 May 2025

Basic Info

Synonyms

ATP-dependent RNA helicase DDX24, DDX24, DEAD box protein 24

+ [1]

Introduction

ATP-dependent RNA helicase that plays a role in various aspects of RNA metabolism including pre-mRNA splicing and is thereby involved in different biological processes such as cell cycle regulation or innate immunity (PubMed:24204270, PubMed:24980433). Plays an inhibitory role in TP53 transcriptional activity and subsequently in TP53 controlled cell growth arrest and senescence by inhibiting its EP300 mediated acetylation (PubMed:25867071). Negatively regulates cytosolic RNA-mediated innate immune signaling at least in part by affecting RIPK1/IRF7 interactions. Alternatively, possesses antiviral activity by recognizing gammaherpesvirus transcripts in the context of lytic reactivation (PubMed:36298642). Plays an essential role in cell cycle regulation in vascular smooth muscle cells by interacting with and regulating FANCA (Fanconi anemia complementation group A) mRNA (By similarity). (Microbial infection) Plays a positive role in HIV-1 infection by promoting Rev-dependent nuclear export of viral RNAs and their packaging into virus particles (PubMed:24204270).

Drugs associated with DDX24

CN118005612

Patent Mining

Target

DDX24

Mechanism-

Active Org.

The Fifth Affiliated Hospital of Sun Yat-sen University

Originator Org.

The Fifth Affiliated Hospital of Sun Yat-sen University

Active Indication

Immunologic Deficiency Syndromes [+2]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with DDX24

100 Translational Medicine associated with DDX24

0 Patents (Medical) associated with DDX24

Literatures (Medical) associated with DDX24

01 Aug 2025·Cellular Signalling

DDX24 inhibits clear cell renal cell carcinoma progression by directly regulating AKR1B10

Article

Author: Li, Zhijun ; Li, Xinglin ; Jin, Hongjun ; Pei, Xiaofeng ; Que, Taotao ; Xian, Jianzhong ; Yang, Min

Clear cell renal cell carcinoma (ccRCC) is one of the most common malignancies worldwide, but only a few markers have been used to diagnose ccRCC. Here, we report the critical roles of DEAD-box helicase 24 (DDX24), a member of the DEAD-box RNA helicase family, in ccRCC. The DDX24 expression level and its prognostic value were initially detected in public data and then verified in a ccRCC tissue microarray. Subsequent in vitro and in vivo experiments were conducted on representative ccRCC cell lines. RNA sequencing and experimental studies were performed to explore the underlying mechanisms, and the associations between DDX24 expression and immune characteristics were evaluated. DDX24 levels were significantly lower in ccRCC tissues and negatively correlated with advanced clinical stage and overall survival. Functional analyses showed that DDX24 overexpression inhibited ccRCC cell proliferation, migration, and invasion, while DDX24 knockdown enhanced these phenotypes. Mechanistic studies revealed that DDX24 regulated the expression of aldo-keto reductase family 1 member B10 (AKR1B10) and epithelial-mesenchymal transition (EMT)-related transcription factors. Given the low expression of DDX24, ccRCC patients may benefit more from immunotherapies. In conclusion, these findings demonstrate that DDX24 suppresses ccRCC progression through direct regulation of AKR1B10, potentially mediated by EMT-related pathways, which provides potential therapeutic targets for ccRCC.

01 Apr 2025·Molecular Biotechnology

Integrative Analyses of Bulk and Single-Cell RNA Seq Identified the Shared Genes in Acute Respiratory Distress Syndrome and Rheumatoid Arthritis

Article

Author: Chen, Wei ; Zhang, Chunyang ; Liu, Lu ; Tang, Jiajia ; Chen, Xuxin ; Qi, Man ; Shi, Jun ; Han, Zhihai

Acute respiratory distress syndrome (ARDS), a progressive status of acute lung injury (ALI), is primarily caused by an immune-mediated inflammatory disorder, which can be an acute pulmonary complication of rheumatoid arthritis (RA). As a chronic inflammatory disease regulated by the immune system, RA is closely associated with the occurrence and progression of respiratory diseases. However, it remains elusive whether there are shared genes between the molecular mechanisms underlying RA and ARDS. The objective of this study is to identify potential shared genes for further clinical drug discovery through integrated analysis of bulk RNA sequencing datasets obtained from the Gene Expression Omnibus database, employing differentially expressed genes (DEGs) analysis and weighted gene co-expression network analysis (WGCNA). The hub genes were identified through the intersection of common DEGs and WGCNA-derived genes. The Random Forest (RF) and least absolute shrinkage and selection operator (LASSO) algorithms were subsequently employed to identify key shared target genes associated with two diseases. Additionally, RA immune infiltration analysis and COVID-19 single-cell transcriptome analysis revealed the correlation between these key genes and immune cells. A total of 59 shared genes were identified from the intersection of DEGs and gene clusters obtained through WGCNA, which analyzed the integrated gene matrix of ALI/ARDS and RA. The RF and LASSO algorithms were employed to screen for target genes specific to ALI/ARDS and RA, respectively. The final set of overlapping genes (FCMR, ADAM28, HK3, GRB10, UBE2J1, HPSE, DDX24, BATF, and CST7) all exhibited a strong predictive effect with an area under the curve (AUC) value greater than 0.8. Then, the immune infiltration analysis revealed a strong correlation between UBE2J1 and plasma cells in RA. Furthermore, scRNA-seq analysis demonstrated differential expression of these nine target genes primarily in T cells and NK cells, with CST7 showing a significant positive correlation specifically with NK cells. Beyond that, transcriptome sequencing was conducted on lung tissue collected from ALI mice, confirming the substantial differential expression of FCMR, HK3, UBE2J1, and BATF. This study provides unprecedented evidence linking the pathophysiological mechanisms of ALI/ARDS and RA to immune regulation, which offers novel understanding for future clinical treatment and experimental research.

02 Jan 2025·Theranostics

Loss of DDX24 inhibits lung cancer progression by stimulating IKBKG splicing-mediated autophagy

Article

Author: Qi, Yangfan ; Sun, Bing ; Tong, Guangquan ; Wang, Chong ; Jing, Xiaomeng ; Zhang, Jinrui ; Sun, Siwen ; Lv, Yuesheng ; Zhang, Wenjing ; Wang, Yang ; Zhang, Ge ; Liu, Congcong ; Xie, Shuaijun ; Chen, Chaoqun ; Chen, Dan ; Zhao, Jinyao

Rationale: Lung cancer remains a major global health burden with limited therapeutic options. Alternative splicing, a critical post-transcriptional process, contributes to lung cancer progression through autophagy, although the underlying mechanisms remain largely unexplored. This study aims to elucidate the role of DDX24 as a splicing factor that contributes to lung cancer progression via autophagy. Methods: To establish the link between DDX24 and lung cancer progression, we performed colony formation assays, growth curve analyses, and xenograft tumor models in nude mice. Mass spectrometry and RNA sequencing were employed to investigate the involvement of DDX24 in alternative splicing, with a specific focus on the splicing of IKBKG. The mechanisms by which DDX24 regulates autophagy were further explored using co-immunoprecipitation and luciferase reporter assays. Results: The splicing factor DDX24 is significantly elevated in lung cancer tissues. Loss of DDX24 suppresses lung cancer growth by promoting autophagy. We identified DDX24 as a splicing factor that plays critical roles in the regulation of alternative splicing. Mechanistically, DDX24 regulates the alternative splicing of autophagy-related genes, including IKBKG. We demonstrate that DDX24 directly binds to IKBKG pre-mRNA, whereas DDX24 ablation stimulates the generation of the long splicing isoform of IKBKG, thereby promoting autophagy through activating of the NF-kB signaling pathway and the transcription of the BECN1 gene. Functional rescue experiments confirm that the long IKBKG isoform-mediated autophagy confers the anti-tumor effects of DDX24 depletion. In addition, IKBKG-L is positively associated with improved survival in lung cancer patients. Conclusions: This study uncovers a novel regulatory axis involving DDX24, IKBKG splicing, and autophagy in lung cancer. Our findings suggest that targeting DDX24 may represent a promising therapeutic strategy for lung cancer treatment, offering new insights into the molecular underpinnings of this disease.

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DDX24

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