Dhx32, also known as DEAH-box polypeptide 32, is an RNA helicase. It is involved in multiple RNA-associated biological processes such as ribosome biosynthesis, transcription, mRNA splicing and translation [5].

In cancer research, in liver cancer, silencing Dhx32 enhanced the proliferative potential of liver cancer cells, with upregulated phosphorylated levels of extracellular signal-regulated kinase (ERK) and protein kinase B (Akt), and increased cyclin-dependent kinases 6 (CDK6) level, indicating its proliferation-suppressing property [1]. In breast cancer, increased Dhx32 expression was associated with poor prognosis and was an independent prognostic factor for decreased overall and disease-free survival [2]. In colorectal cancer, Dhx32 promoted angiogenesis by upregulating vascular endothelial growth factor A (VEGFA) through interacting with and stabilizing β-catenin, and its depletion reduced microvessel density and suppressed tumor growth; overexpressed Dhx32 also promoted cancer cell proliferation, migration, invasion and decreased chemotherapy susceptibility, and its depletion affected the expression of genes in the Wnt pathway and apoptosis-related genes [3,4]. In hepatocellular carcinoma, high Dhx32 expression was associated with reduced overall survival, and its ectopic expression induced epithelial-mesenchymal transition (EMT), promoted cell mobility, proliferation and tumour growth, while silencing Dhx32 reversed these effects and was related to β-catenin in the nucleus [6].

In conclusion, Dhx32 is a crucial RNA helicase involved in various biological processes related to RNA. Its role in cancer, especially in liver, breast, colorectal and hepatocellular carcinoma, has been revealed through functional studies including gene silencing. These findings suggest that Dhx32 may serve as a potential biomarker and therapeutic target for these cancers.