Ask about this productRelated genes to: SNRPF antibody
- Gene:
- SNRPF NIH gene
- Name:
- small nuclear ribonucleoprotein polypeptide F
- Previous symbol:
- -
- Synonyms:
- Sm-F
- Chromosome:
- 12q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-13
- Date modifiied:
- 2011-10-11
Related products to: SNRPF antibody
Related articles to: SNRPF antibody
- Ovarian cancer (OC) remains a major cause of gynecologic cancer mortality, with progress in targeted therapy limited by an incomplete understanding of post-transcriptional oncogenic drivers. Dysregulated RNA splicing-particularly intron retention (IR)-is increasingly recognized as a key driver of tumor progression. Here, integrated transcriptomic and proteomic analyses identify SNRPF, a core spliceosomal component, as a potent oncogenic driver in OC. SNRPF is highly expressed in tumor specimens, and its overexpression predicts poor patient survival. Silencing SNRPF suppresses proliferation, invasion, and xenograft growth. IR-focused analysis reveals that SNRPF depletion induces intron 6 retention in DDX24, disrupting the Helicase_C domain and generating premature termination codons that activate nonsense-mediated decay (NMD), thereby reducing DDX24 protein abundance and markedly impairing its oncogenic function. DDX24 depletion similarly promotes intron 2 retention in E2F4, causing NMD-mediated downregulation. Notably, E2F4 directly binds the SNRPF promoter, forming a self-sustaining "SNRPF-DDX24-E2F4" axis linking splicing and transcriptional regulation. Antisense oligonucleotide-mediated inhibition of SNRPF disrupts this feedback loop, downregulates DDX24 and E2F4 via IR, and significantly impairs tumor growth in vitro, in vivo, and in patient-derived xenografts. These findings define a splicing-transcription coupling mechanism in OC and position SNRPF as a promising therapeutic target. - Source: PubMed
Publication date: 2026/05/10
Li YingweiChen ZhongshaoGao QianqianGao YuehanYang Ning - The Solute carrier family 25 member 3 (SLC25A3), a mitochondrial solute carrier protein, has been implicated in tumor progression. Nonetheless, the connection between SLC25A3 and hepatocellular carcinoma (HCC) remains ambiguous. - Source: PubMed
Publication date: 2026/01/24
Bie BeibeiLiu LibingWang FurongMeng XianingWu MengdiSun Jin - Spliceosome abnormalities are implicated in hepatocellular carcinoma (HCC) pathogenesis, but the role of the core component small nuclear ribonucleoprotein polypeptide F (SNRPF) remains unclear. This study aims to elucidate the role and mechanism of SNRPF in HCC progression. SNRPF expression and clinical significance were analyzed using the DepMap and TCGA databases, alongside clinical HCC specimens. The results revealed that SNRPF was essential for HCC cell proliferation (CERES score = -3.02) and aberrantly overexpressed in HCC, correlating with poor prognosis. Functional validation via overexpression or knockdown in HCC cells demonstrated that SNRPF significantly promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Mechanistically, RNA immunoprecipitation and reporter gene assays showed SNRPF bound to the pre-mRNA of transmembrane P24 trafficking protein 2 (TMED2), preventing its Intron 2 retention and subsequent nonsense-mediated decay, thereby ensuring TMED2 protein abundance. Co-immunoprecipitation and GST pull-down assays revealed that TMED2 directly interacted with cGAS, promoting its activation and the subsequent STING/TBK1/IRF3 signaling cascade. This activation induced elevated levels of IFN-β, ISG15, and IFIT1/2, as well as the secretion of IFN-β, TNF-α, and IL-6. Rescue experiments using cGAS or STING inhibitors confirmed these findings. In vivo experiments using an orthotopic xenograft tumor model in mice further confirmed that the SNRPF/TMED2/cGAS-STING axis significantly promotes the growth and progression of HCC tumors. In conclusion, this study elucidates the pivotal oncogenic function of the SNRPF/TMED2/cGAS-STING signaling axis in HCC, providing novel strategies for prognosis prediction and targeted therapy. - Source: PubMed
Publication date: 2026/03/03
Xie XiaocuiPu LinglingZeng JiangXu MengyueYin XiaofeiLiu HuaYang JingCao JinmingSong Haixing - The causal association between plasma proteomes and the risk of developing hepatocellular carcinoma (HCC) in human populations has not been fully elucidated. Mendelian randomization (MR) is an innovative epidemiological study design that enables the unbiased identification of causal relationships by utilizing genetic variants as instrumental variables. Consequently, we employed a two-sample MR approach to investigate the potential causal link between plasma protein levels and the incidence of HCC. A comprehensive bidirectional two-sample MR analysis was performed using genome-wide significant published genome-wide association studies of plasma proteomes (N: 35,559 healthy individuals) and HCC (168 cases and 372,016 controls). Sensitivity analyses were conducted for identified causal proteins. Furthermore, we pursued pathway exploration using Kyoto Encyclopedia of Genes and Genomes and gene ontology analyses. Protein-protein interaction network analysis provided insights into plasma protein-HCC interactions. We identified 17 plasma proteins causally associated with HCC risk (PIVW < .05). Sixteen proteins were positively associated, including TMCC3, METTL1, SNRPF, KRT19, MED4, RFNG, IL26, NRXN1, MSH2, CLCA2, AKT2, CRYZL1, RDH16, CSF3, CPA4 and COPS7B, while EPHA2 was inversely associated. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses implicated key gene correlations with JAK-STAT, PI3K-AKT and chemokine pathways. The protein-protein interaction network highlighted potential plasma protein-HCC relationships. Our genetics-based approach provides evidence supporting a causal role for specific plasma proteomes in influencing HCC risk. Results support causal effects on HCC for TMCC3, METTL1, SNRPF, KRT19, MED4, RFNG, IL26, NRXN1, MSH2, CLCA2, AKT2, CRYZL1, RDH16, CSF3, CPA4, EPHA2, and COPS7B. Experimental validation and mechanistic study are warranted to confirm findings. - Source: PubMed
Chen XueZheng ZhenHu JingYe ShuangLiu Kaitai - The comorbidity of atherosclerosis (AS) and depression presents a significant clinical challenge. Its pathogenesis entails complex abnormalities in inflammatory responses, lipid metabolism, and gut microbiota homeostasis. Ginsenoside Rb1 (GRb1)-a bioactive compound derived from the dried roots of Panax ginseng (Araliaceae)-demonstrates anti-inflammatory, antioxidant, lipid-lowering, and neuroprotective properties. However, GRb1's therapeutic potential and underlying mechanisms in AS co-depression remain inadequately characterized. - Source: PubMed
Publication date: 2025/09/22
Zhao YulongSong TaoRen PengWu XiaoyunLuo QiangXie JingLai HouminLi XueWen YouliangLiao XingxingZhou Junjie