Ddx60, an interferon-inducible cytoplasmic helicase, is involved in multiple biological processes. It plays a role in antiviral innate immune responses, such as being a sentinel for RIG-I activation and viral RNA degradation, and is also associated with various signaling pathways like the AKT-GSK3β-STAT3 pathway, NF-κB/IFI27 axis [1,6]. It is of great biological importance as it impacts immune responses, cell proliferation, migration, and invasion, thus having implications for cancer and autoimmune diseases.

In cancer research, loss-of-function studies in various models have provided insights. In colorectal cancer, oncogenic KRAS down-regulates Ddx60, accelerating dsRNA degradation and impairing the IFN response, while overexpressing Ddx60 reactivates IFN signaling and increases sensitivity to immune checkpoint inhibition therapy [1]. In head and neck squamous cell carcinoma, Ddx60 promotes cell migration and invasion through the NF-κB/IFI27 signaling pathway [3]. In pancreatic cancer, Ddx60 is upregulated, promoting cell proliferation, migration, and invasion, and is related to poor prognosis and immune resistance [5]. In glioma, Ddx60 is upregulated and has prognostic value, being associated with the inflammatory and immune response [4]. In breast cancer, low expression of Ddx60 might associate with radiosensitivity [7]. In the context of exercise hypertrophic preconditioning, silencing of circ-Ddx60 (derived from Ddx60) attenuated the antihypertrophic effect in mice [2].

In conclusion, Ddx60 is crucial in antiviral immunity and has significant impacts on multiple diseases, especially cancers. Studies using gene knockout or other loss-of-function models have revealed its role in regulating immune responses, cell behaviors, and disease progression, providing potential therapeutic targets for various diseases including cancer and autoimmune disorders.