ArticleMolecular therapy. Nucleic acids2021
CD46 splice variant enhances translation of specific mRNAs linked to an aggressive tumor cell phenotype in bladder cancer.
Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- From cell lines to the clinic: identifying a urinary BlCa-EV signature through comparative proteomics of bladder cancer lysates and extracellular vesicles.Cell communication and signaling : CCS · 2026Article
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- The multiverse of CD46 and oncologic interactions.The Journal of clinical investigation · 2025Review
- Complement regulatory protein CD46 promotes bladder cancer metastasis through activation of MMP9.International journal of oncology · 2024Article
- Review
- Alternative splicing regulation and its therapeutic potential in bladder cancer.Frontiers in oncology · 2024Review
- Complement System and the Kidney: Its Role in Renal Diseases, Kidney Transplantation and Renal Cell Carcinoma.International journal of molecular sciences · 2023Review
- Complosome - the intracellular complement system.Nature reviews. Nephrology · 2023Review
- A comprehensive understanding of hnRNP A1 role in cancer: new perspectives on binding with noncoding RNA.Cancer gene therapy · 2023Review
- RNA-Binding Proteins in Bladder Cancer.Cancers · 2023Review
- Heterogeneous nuclear ribonucleoprotein A/B: an emerging group of cancer biomarkers and therapeutic targets.Cell death discovery · 2022Review
- hnRNP A1 in RNA metabolism regulation and as a potential therapeutic target.Frontiers in pharmacology · 2022Review
- Comprehensive Analysis of Prognostic Alternative Splicing Signature Reveals Recurrence Predictor for Papillary Thyroid Cancer.Frontiers in oncology · 2021Article
- Dysregulation of mRNA splicing in urothelial carcinoma: Clinical, diagnostic and therapeutic implications.Bladder cancer (Amsterdam, Netherlands)Review
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD46 is well known to be involved in diverse biological processes. Although several splice variants of CD46 have been identified, little is known about the contribution of alternative splicing to its tumorigenic functions. In this study, we found that exclusion of CD46 exon 13 is significantly increased in bladder cancer (BCa) samples. In BCa cell lines, enforced expression of CD46-CYT2 (exon 13-skipping isoform) promoted, and CD46-CYT1 (exon 13-containing isoform) attenuated, cell growth, migration, and tumorigenicity in a xenograft model. We also applied interaction proteomics to identify exhaustively the complexes containing the CYT1 or CYT2 domain in EJ-1 cells. 320 proteins were identified that interact with the CYT1 and/or CYT2 domain, and most of them are new interactors. Using an internal ribosome entry site (IRES)-dependent reporter system, we established that CD46 could regulate mRNA translation through an interaction with the translation machinery. We also identified heterogeneous nuclear ribonucleoprotein (hnRNP)A1 as a novel CYT2 binding partner, and this interaction facilitates the interaction of hnRNPA1 with IRES RNA to promote IRES-dependent translation of HIF1a and c-Myc. Strikingly, the splicing factor SRSF1 is highly correlated with CD46 exon 13 exclusion in clinical BCa samples. Taken together, our findings contribute to understanding the role of CD46 in BCa development.
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