DDX24 Mutations Associated With Malformations of Major Vessels to the Viscera

Pang, Pengfei; Hu, Xiaojun; Zhou, Bin; Mao, Junjie; Yu, Liang; Jiang, Zai-bo; Huang, Mingsheng; Liu, Ruihong; Zhang, Youyong; Qian, Ji; Liu, Jinsong; Xu, Jinxin; Zhang, Yaqin; Zu, Maoheng; Wang, Yiming; He, Huanhuan; Shan, Hong

doi:10.1002/hep.30200

Cited by 9 publications

(12 citation statements)

References 45 publications

(69 reference statements)

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“… 29 Our previous research revealed that DDX24 mutations were pathogenic factors of vascular deformities and played a significant role in the migration ability of endothelial cells. 10 Based on published reports, DDX24 functions as a modulator of the p300-p53 axis by suppressing the p300-mediated acetylation of p53, which promotes the proliferation of osteosarcoma cells and lung carcinoma cells. 11 Additionally, other studies revealed that a perturbation of DDX24 inhibited colon cancer and gastric cancer growth.…”

Section: Discussionmentioning

confidence: 99%

“… 8 DDX24 is an important member of the DEAD-box RNA helicases carrying a conserved Asp-Glu-Ala-Asp (D-E-A-D) motif. 9 Based on our recent findings, a mutated DDX24 gene could cause vascular malformations, 10 and previous studies have revealed that DDX24 is upregulated in multiple human cancer cells, inhibiting cell growth by inducing cell cycle arrest and senescence in osteosarcoma cells. 11 Moreover, DDX24 also regulates the proliferation of colon cancer and gastric cancer cells.…”

Section: Introductionmentioning

confidence: 94%

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DDX24 regulates the chemosensitivity of hepatocellular carcinoma to sorafenib via mediating the expression of SNORA18

Gan

et al. 2022

Cancer Biology & Therapy

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Sorafenib (SFN) is a multi-kinase inhibitor drug for the treatment of advanced hepatocellular carcinoma (HCC), but its limited efficacy is a major obstacle to the clinical outcomes of patients with HCC. We aimed to explore a novel molecular mechanism underlying the chemosensitivity of HCC to SFN, and to identify a promising therapeutic target for HCC treatment. In this study, bioinformatic analysis revealed that DDX24 was associated with poor survival in HCC cases, and significantly related to the pathways modulating tumor development. DDX24 regulated HCC cell proliferation and migration potentials. Moreover, reduction of DDX24 promoted the sorafenib-mediated inhibition of HCC cell growth and migration, the elevation of sorafenib-induced HCC cell apoptosis. DDX24 overexpression suppressed the inhibitory effect of SFN on cell proliferation and migration and reduced the apoptosis induced by SFN. Further, DDX24, combined with SFN treatment, presented a synergistic enhancement of the sensitivity of SFN to the growth and migration of HCC cells via AKT/ERK and the epithelial-mesenchymal transition (EMT) pathways, and that it modulated apoptosis via the caspase/PARP pathway. Mechanistically, SNORA18 served as a target gene for DDX24, regulating the chemosensitivity of sorafenib-treated HCC cells. Furthermore, SNORA18 knockdown or overexpression could partially reverse the inhibition or elevation of cell viability, colony formation and migration induced by DDX24 in sorafenib-treated HCC cells, respectively. Collectively, our results suggest that DDX24 regulates the chemosensitivity of HCC to SFN by mediating the expression of SNORA18, which may act as an effective therapeutic target for improving SFN efficiency in HCC treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

DDX24 regulates the chemosensitivity of hepatocellular carcinoma to sorafenib via mediating the expression of SNORA18

Gan

et al. 2022

Cancer Biology & Therapy

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“…Using cell culture models and zebrafish knockouts they determined that single nucleotide polymorphism mutations in DDX24, a gene coding for a DEAD box helicase, are responsible not only for the MOVLD syndrome but could also be found in some sporadic cases of vascular malformation, and that DDX24 is involved in early vascular development. 18 In this patent document the inventors proceed to identify antagonists of the cysteinyl leukotriene receptor-1 as agents to treat or prevent such malformations. These are the asthma drugs based on the ''lukast'' class of agents (motelukast, zafirlukast, and pranlukast) but also the older necrodomil.…”

Section: A Nonresorbable Antibiotic Prevents Sickle Cell Vaso-occlusive Crisesmentioning

confidence: 99%

Drug Repurposing Patent Applications October–December 2020

Mucke¹

2021

ASSAY and Drug Development Technologies

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“… 10 , 11 In previous studies, DDX24 was associated with cancer development, 12 viral infection, 13 and vascular malformation. 14 However, the role of DDX24 in developing different tumors was complicated, 6 , 15 and the correlation between DDX24 and NSCLC remains unclear and requires further investigation.…”

Section: Introductionmentioning

confidence: 99%

DDX24 promotes metastasis by regulating RPL5 in non‐small cell lung cancer

Zhou

et al. 2022

Cancer Medicine

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Purpose: Non-small cell lung cancer (NSCLC) is a leading cause of cancer death, and metastasis is a crucial determinant of increased cancer mortality. DDX24 has garnered increased attention due to its correlation with tumorigenesis and malignant progression. However, the correlation between DDX24 and NSCLC remains unclear.Methods: DDX24 expression in NSCLC tissues and survival rate of patients was analyzed using bioinformatic analysis. Transwell assays, wound-healing assays, and tail vein lung colonization models were employed to determine the role of DDX24 in migration and invasion in vitro and in vivo. We searched for DDX24interacting proteins using co-immunoprecipitation followed by mass spectroscopy and verified the interaction. The influence of DDX24 on RPL5 expression and ubiquitination was examined using protein stability assays.Results: DDX24 expression was upregulated in NSCLC cell lines and tumors of patients, particularly those with high tumor grades. A high DDX24 level was also correlated with a poor prognosis. DDX24 upregulation enhanced the migration and invasion ability of NSCLC cells, whereas its downregulation had the opposite effects. In vivo xenograft experiments confirmed that tumors with high DDX24

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DDX24 Mutations Associated With Malformations of Major Vessels to the Viscera

Cited by 9 publications

References 45 publications

DDX24 regulates the chemosensitivity of hepatocellular carcinoma to sorafenib via mediating the expression of SNORA18

DDX24 regulates the chemosensitivity of hepatocellular carcinoma to sorafenib via mediating the expression of SNORA18

Drug Repurposing Patent Applications October–December 2020

DDX24 promotes metastasis by regulating RPL5 in non‐small cell lung cancer

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