Abnormal RNA metabolism is one of the core mechanisms in tumorigenesis. DDX23, a member of the family of DEAD-box protein, characterized as an ATP-dependent RNA helicase, facilitates cancer progression due to its abnormal expression. However, systematic studies examining DDX23 across the pan-cancer spectrum remain scarce. We utilized databases like TCGA and GEO to thoroughly examine the expression pattern of DDX23 in our study, its prognostic value, diagnostic efficacy, and immune-related properties across multiple cancers. We foresee possible regulatory routes by building a network of protein interactions and performing analysis of functional enrichment. Concurrently, we validate the core biological functions of DDX23 through in vitro experiments. DDX23 demonstrates markedly increased expression across a majority types of cancer, and its overexpression is strongly tied to a negative patient outcome. The level of DDX23 expression is closely linked to tumor mutational burden and the presence of infiltrating immune cells. Functional enrichment analysis indicates that DDX23 primarily participates in pathways related to RNA splicing and cell proliferation. In breast cancer (BRCA) tissue, DDX23 expression is notably higher than in normal breast tissue. In vitro experiments provide additional confirmation that DDX23 substantially boosts breast cancer cells’ ability to proliferate, invade, and migrate. In this investigation, DDX23 has been identified as a crucial biological marker for forecasting survival outcomes and immunological overview in patients with various types of cancer. It clarifies its specific expression pattern and oncogenic function in BRCA, providing crucial evidence for its clinical application in BRCA-targeted therapy and highlighting its translational potential.
Ma et al. (Wed,) studied this question.