Ask about this productRelated genes to: SF3B3 Blocking Peptide
- Gene:
- SF3B3 NIH gene
- Name:
- splicing factor 3b subunit 3
- Previous symbol:
- -
- Synonyms:
- SAP130, SF3b130, RSE1, KIAA0017
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-29
- Date modifiied:
- 2016-10-05
Related products to: SF3B3 Blocking Peptide
Related articles to: SF3B3 Blocking Peptide
- O-GlcNAcylation is a post-translational modification (PTM) uniquely catalyzed by O-GlcNAc transferase (OGT), which has been linked to tumorigenesis and neurodegeneration. However, its roles in mammalian spermatogenesis remain unexplored. This study aims to elucidate the functional mechanisms of OGT in spermatogenesis and male fertility. - Source: PubMed
Publication date: 2026/07/03
Ding ZhimingWu CaiyunLi MinHu KaiqinLi XuanxiChen ZhenLi KuokuoCheng HuiruShen QunshanCao YunxiaXiang HuifenGuo Rui - Alternative splicing dysregulation contributes to colorectal cancer (CRC) progression, yet the roles of specific splicing factors, such as SF3B3, remain poorly defined. To identify key dysregulated splicing factors, RNA sequencing was performed comparing high-metastatic (SW620) and low-metastatic (SW480) CRC cell lines. Notably, SW480 and SW620 are isogenic cell lines derived from the primary tumor and lymph node metastasis of the same CRC patient, respectively. Their consistent genetic background minimizes confounding factors, enabling reliable detection of metastasis-associated molecular alterations. Functional assays-including MTT, wound healing, and transwell experiments-combined with molecular analyses confirmed the critical role of the SF3B3-STOX1 axis. SF3B3 was markedly upregulated in metastatic CRC cells and patient tissues. Mechanistically, SF3B3 promoted CRC cell proliferation, migration, and invasion by modulating STOX1 alternative splicing, specifically enhancing exon 3 inclusion to produce the oncogenic isoform STOX1-L while suppressing STOX1-S. Notably, STOX1-L, but not STOX1-S, robustly activated the PI3K-AKT and MAPK/ERK signaling pathways. Importantly, knockdown of STOX1-L reversed the malignant phenotypes driven by SF3B3. Collectively, these results identify SF3B3 as a pivotal regulator of CRC cell metastasis in the isogenic SW480/SW620 cell model that acts through the production of STOX1-L, establishing the SF3B3-STOX1-L axis as a promising candidate therapeutic target for advanced colorectal cancer worthy of further validation in diverse CRC models. - Source: PubMed
Publication date: 2026/06/26
Zhou LiliGuo ZhongxueYu LiuTraore Aime Gael YayaYu ZiqingHuang QiuxueCao YutingZheng QingWang Feng - Urothelial bladder cancer (UBC) poses a considerable threat to public health, and its clinical management is limited by high recurrence rates and a tendency for progression. While dysregulation of the ubiquitin‒proteasome system (UPS) is a hallmark of tumorigenesis, the specific landscape of deubiquitinating enzymes (DUBs) in UBC remains largely underexplored. Multiple transcriptomic datasets were used for a comprehensive screening of ubiquitination-related genes in UBC, and ZRANB1 was identified as a potential oncogenic DUB, whose expression was validated using immunohistochemistry. High ZRANB1 expression was correlated with advanced pathological T stage, lymph node metastasis, and poor overall survival. The oncogenic role of ZRANB1 was assessed by proliferation, migration, and invasion assays in vitro, as well as in subcutaneous xenograft and lymph node metastasis models in vivo. Using immunoprecipitation coupled with mass spectrometry, we revealed that ZRNAB1 acted as a DUB to prevent the UPS-dependent degradation of SF3B3. The ZRANB1-SF3B3 axis subsequently modulates the alternative splicing of the cell cycle checkpoint kinase CHEK2, specifically inhibiting the production of the exon 4-skipped isoform (CHEK2-e4-). We demonstrated that while full-length CHEK2 is permissive for growth, the CHEK2-e4- isoform exerts a potent tumour-suppressive effect. This study reveals a novel post-translational mechanism linking the UPS to the RNA splicing machinery in UBC. ZRANB1 promotes tumorigenesis by stabilizing SF3B3 to prevent the generation of the tumour-suppressive CHEK2-e4- isoform, suggesting that ZRANB1 is a promising prognostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/06/09
Yan DongZhu WenjieTao YiranHuang LifangZhang YunlongZhu WenliangHe QingqingWang DejuanQiu Jianguang - Protein kinases play a crucial role in regulating cellular processes, and their dysregulation is frequently implicated in various diseases, including cancer. Targeting protein kinases represents a promising therapeutic strategy for cancer treatment. Esophageal squamous cell carcinoma (ESCC) constitutes over 90% of esophageal cancer cases in high-incidence regions, with a global five-year survival rate below 20%. Here, we report that CK2 is aberrantly activated in ESCC, identified through kinase-substrate enrichment analysis (KSEA) of large-scale proteomic and phosphoproteomic data. Functional enrichment revealed the splicing factor SF3B3 as a clinically relevant CK2 substrate. We demonstrated that CK2-mediated phosphorylation of SF3B3 T1200 plays a pivotal role in ESCC progression. Mechanistically, CK2-mediated phosphorylation of SF3B3 enhances its affinity for the deubiquitinase USP7, leading to SF3B3 deubiquitination and subsequent protein stabilization. This stabilization drives ESCC progression by regulating alternative splicing (AS) events, including a critical event involving the inclusion of exon 4 in the EXOSC2 transcript. Furthermore, we demonstrated that SF3B3 T1200 phosphorylation specifically facilitates its incorporation into the U2 snRNP complex, directly promoting the aforementioned EXOSC2 exon 4 inclusion. Crucially, targeting CK2 or USP7, either individually or in combination, effectively suppressed ESCC progression. Our findings uncover a key molecular mechanism underlying SF3B3 stabilization and AS regulation, offering novel therapeutic opportunities for ESCC. - Source: PubMed
Publication date: 2026/04/10
Wang Du-ChuangLi Jia-YuanWang Xiao-BingHu Guo-ShengNie Rui-ChaoZheng BinHe Yao-HuiLiu Wen - BACKGROUND: Atherosclerosis (AS) is a chronic inflammatory disease that compromises vascular health and underlies major cardiovascular events. SF3B3, a core spliceosome component, mediates exon–intron processing, yet its role in AS remains unclear. METHODS: We performed integrative analyses of differentially expressed genes across GEO datasets (GSE43292 and GSE9820) and immune-related gene sets from ImmPort. Feature selection was refined using LASSO regression and SVM-RFE. Functional enrichment was assessed via GSEA and GSVA, while immune associations were evaluated with CIBERSORT and ESTIMATE. Key findings were validated in an independent dataset (GSE9820). RESULTS: Thirteen hub genes associated with SF3B3 were identified. SF3B3 expression correlated with enhanced antiviral defense, cytokine production, and immune signaling pathways. Higher SF3B3 levels were positively associated with adaptive immune populations—including memory and naïve B cells, CD4⁺ and CD8⁺ T cells, follicular helper T cells, and regulatory T cells—while inversely correlated with activated memory CD4⁺ T cells, monocytes, macrophages, eosinophils, and activated dendritic cells. CONCLUSIONS: SF3B3 is closely linked to immune infiltration patterns in AS, highlighting its potential as a biomarker and a candidate target for therapeutic intervention. These findings provide a framework for future mechanistic studies and clinical applications. - Source: PubMed
Publication date: 2026/04/07
Yang NanLiu JifangZhang QianqianJiang DongliZheng ManGuo ZhongxiuWang Zongtao