ArticleCancer science2024
SYT4 binds to SNAP25 to facilitate exosomal secretion and prostate cancer enzalutamide resistance.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Integrative RNA-Seq and TCGA-BRCA Analyses Highlight the Role of LINC01133 in Triple-Negative Breast Cancer.Biomedicines · 2026Article
- Prognostic value of vascular endothelial growth factor subtypes and risk models constructed based on the common pathway of ulcerative colitis and colon cancer.Open medicine (Warsaw, Poland) · 2026Article
- PDGFC facilitates enzalutamide resistance in prostate cancer through activation of the Rap1-MAPK pathway.Journal of cancer research and clinical oncology · 2025Article
- SYT4 Interacts with PSMC6 to Facilitate Malignant Progression in Gastric Carcinoma via Activating Wnt/β-catenin Signaling.International journal of biological sciences · 2025Article
- SYT4 binds to SNAP25 to facilitate exosomal secretion and prostate cancer enzalutamide resistance.Cancer science · 2024Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Prostate carcinoma represents a predominant malignancy affecting the male population, with androgen deprivation therapy (ADT) serving as a critical therapeutic modality for advanced disease states, but it often leads to the development of resistance. Enzalutamide (Enz), a second-generation antiandrogen drug, initially offers substantial therapeutic benefit, but its efficacy wanes as drug resistance ensues. In this study, we found that synaptotagmin 4 (SYT4) is an upregulated gene in enzalutamide-resistant (EnzR) cell lines. The downregulation of SYT4, in combination with enzalutamide therapy, substantially enhances the antiproliferative effect on resistant prostate cancer cells beyond the capacity of enzalutamide monotherapy. SYT4 promotes vesicle efflux by binding to the synaptosome-associated protein 25 (SNAP25), thereby contributing to cell resistance against enzalutamide. The elevated expression of SYT4 is mediated by bromodomain-containing protein 4 (BRD4), and BRD4 inhibition effectively suppressed the expression of SYT4. Treatment with a therapeutic dose of enzalutamide combined with ASO-1, an antisense oligonucleotide drug targeting SYT4, shows promising results in reversing the resistance of prostate cancer to enzalutamide.
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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 Socratic graph.