Ddx55, a DEAD-box helicase, is involved in diverse biological processes. It plays a role in ribosome biogenesis, being recruited to domain IV of the 28S ribosomal RNA by its C-terminal region and is required for maturation of large subunit pre-rRNAs [2]. It may also be involved in mitochondrial splicing as suggested by a study on T-2 toxin-induced mitochondrial biogenesis [6].

In hepatocellular carcinoma (HCC), Ddx55 is upregulated. It promotes HCC cell proliferation, migration, and invasion both ex vivo and in vivo. Mechanistically, it interacts with BRD4 to form a transcriptional regulatory complex that positively regulates PIK3CA transcription, activating β-catenin signaling in a PI3K/Akt/GSK-3β dependent manner, thus inducing cell cycle progression and epithelial-mesenchymal transition. Also, exosomal DDX55 participates in intercellular communication between HCC cells and endothelial cells, promoting the malignant phenotype of HCC cells and angiogenesis. Ddx55 is identified as a valuable prognostic biomarker and therapeutic target in HCC [1].

In lung cancer, Ddx55 is a negative prognostic factor, and its high expression is associated with high levels of TP53 and MUC16 mutation [5].

In addition, in severe COVID-19, lower levels of Ddx55 in plasma before mesenchymal stem cell (MSC) treatment are predictors of responders to MSC therapy [3]. And in locoregionally advanced nasopharyngeal carcinoma, Ddx55 in plasma may serve as a potential biomarker for early identification of induction chemotherapy beneficiaries [4].

In summary, Ddx55 is crucial in ribosome biogenesis and mitochondrial-related processes. Its role in multiple diseases such as HCC, lung cancer, severe COVID-19, and locoregionally advanced nasopharyngeal carcinoma has been revealed through various studies. Understanding Ddx55's functions in these disease conditions may provide new insights for diagnosis, prognosis, and treatment strategies.