ArticleOncogene2025
SNRPB-mediated regulation of DDX39A splicing promotes ovarian cancer progression by regulating α6 integrin subunit expression.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Integrated genome-wide high-throughput screening and functional validation identifies Sm proteins as essential splicing regulators for gastric cancer progression.Functional & integrative genomics · 2026Article
- Disruption of the SNRPF-DDX24-E2F4 Feedback Loop Uncouples Splicing and Transcriptional Regulation to Suppress Ovarian Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- SNRPD2-mediated regulation of DDX39B splicing promotes endometrial cancer progression by suppressing the activation of CTSC cryptic exons.Cell death & disease · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Dysfunction or aberrant expression of DEAD-box RNA helicases might play a role in the initiation and progression of human cancers. Nevertheless, the key regulator and underlying molecular mechanism have yet to be fully elucidated in ovarian cancer. This study identified DDX39A as one of the prominently upregulated genes in ovarian cancer through a systematic analysis of RNA helicase expression profiles using the CPTAC and TCGA ovarian cancer datasets. High expression of DDX39A was confirmed in paraffin-embedded ovarian cancer samples. Specifically, elevated DDX39A expression was found to be associated with poor overall survival in ovarian cancer patients. Antisense oligonucleotide-mediated DDX39A silencing led to a decrease in the proliferation capacity of a CDX model and a PDX model. Furthermore, DDX39A expression is regulated by the splicing factor SNRPB. SNRPB depletion or DDX39A knockdown induced the retention of DDX39A introns 6 and 8 to generate the noncoding transcript DDX39A-209, which yielded premature termination codons and resulted in nonsense-mediated RNA decay and decreased expression of the DDX39A protein. DDX39A silencing reduced the proliferative and metastatic capacities of SNRPB-overexpressing cells, indicating that DDX39A mediates the oncogenic function of SNRPB in ovarian cancer cells. In addition, RNA-Seq data analysis revealed that DDX39A promotes the proliferation and metastasis of ovarian cancer cells through the regulation of exon skipping of ITGA6 to produce the oncogenic ITGA6A transcript. These findings suggest that the SNRPB/DDX39A/ITGA6 axis plays critically important role in the progression of ovarian cancer, which increases our understanding of the role of DEAD-box RNA helicases and provides a viable therapeutic target for ovarian cancer.
Indexed as
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40216968What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.