Ddx54, also known as Dbp10, is a DEAD-box RNA helicase. It plays essential roles in various biological processes. It is involved in ribosome biogenesis, specifically initiating peptidyl transferase center formation during 60S ribosome biogenesis [4,5]. It also functions as a nucleotide exchange factor for casein kinase 2, stimulating its protein kinase activity [6].

In disease-related studies, in colorectal cancer, Ddx54 is overexpressed. High levels are correlated with tumor stage and distant metastasis, and it promotes CRC cell proliferation and mobility by activating p65 and AKT signaling pathways [1]. In gastric cancer, Ddx54 binds to SNHG10 and PBX3, and SNHG10 maintains PBX3 mRNA stability through recruiting Ddx54, facilitating cell growth [3]. In osteosarcoma, lncRNA CBR3-AS1 recruits Ddx54 to upregulate NUCKS1, activating the mTOR signaling pathway and promoting tumor progression [7]. In multiple sclerosis, oligodendrocyte-specific Ddx54 knockout mice gradually develop myelin-related abnormalities, indicating Ddx54 is indispensable for myelin homeostasis [2].

In summary, Ddx54 is crucial for ribosome biogenesis and acts as a nucleotide exchange factor. Its dysregulation is associated with multiple cancers and a demyelinating disease. Studies using gene knockout models, especially in mice, have revealed its role in these biological processes and disease conditions, providing insights into potential therapeutic strategies.