Ddx52, an ATP-dependent RNA helicase, is involved in multiple biological processes. It has been associated with ribosomal RNA processing, as it maintains the level of 47S precursor ribosomal RNA in zebrafish [3]. It may also participate in regulating P-bodies and microtubules, and is involved in spermatogonial mitosis and spermatid differentiation in Chinese mitten crab [5].

In disease-related studies, Ddx52 shows up-regulation in multiple cancers. In lung adenocarcinoma (LUAD), higher Ddx52 expression is related to advanced T and N stages, higher grading and staging, and it can be an independent prognostic determinant and potential therapeutic target [1]. In prostate cancer (PCa), Ddx52 is overexpressed, and its knockdown inhibits PCa cell growth by regulating c-Myc signaling [2]. Similarly, in melanoma, Ddx52 is overexpressed, and its knockdown suppresses melanoma cell proliferation in vitro and of nude mouse xenografts by targeting c-Myc [4]. In colon cancer, Ddx52 is part of an RNA processing-related prognostic risk model [7]. Also, in a fetus with 17q12 microdeletion, Ddx52 was among the genes in the deleted region [6].

In conclusion, Ddx52 plays crucial roles in normal biological processes such as growth regulation in zebrafish and spermatogenesis in Chinese mitten crab. In disease, especially in multiple cancers, its overexpression is often associated with poor prognosis and tumor progression. These findings from various in vivo models and disease-based studies suggest Ddx52 as a potential biomarker and therapeutic target in certain cancers.