Ask about this productRelated genes to: FUBP3 Blocking Peptide
- Gene:
- FUBP3 NIH gene
- Name:
- far upstream element binding protein 3
- Previous symbol:
- FBP3
- Synonyms:
- -
- Chromosome:
- 9q34.11-q34.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-22
- Date modifiied:
- 2018-02-13
Related products to: FUBP3 Blocking Peptide
Related articles to: FUBP3 Blocking Peptide
- Far upstream element binding protein (FUBP)3, a member of the FUBP family of proteins, is a DNA-binding transcription activator and an RNA-binding protein. FUBP3 is deregulated in various types of human cancer and promotes cell proliferation. However, the underlying molecular mechanism of FUBP3 in cancer is still unclear. Therefore, the present study investigated the cell biology, gene expression profile and alternative splicing pattern of HeLa and Huh7 cells following FUBP3 knockdown, in comparison with control cells. The results showed that FUBP3 knockdown promoted proliferation and inhibited apoptosis of HeLa cells, but inhibited the proliferation of Huh7 cells. FUBP3 knockdown markedly affected the transcriptional level of genes involved in cell adhesion, cell proliferation and the apoptotic process. Furthermore, FUBP3 broadly regulated the alternative splicing of hundreds of genes with functions in cellular component disassembly and the apoptotic process. Validation experiments using reverse transcription-quantitative PCR demonstrated that FUBP3 regulated the expression and alternative splicing of genes associated with cell adhesion, cell proliferation and apoptosis in the HeLa and Huh7 cells lines. These results indicated that FUBP3 could regulate the proliferation and apoptosis of cancer cells perhaps via different gene expression and splicing regulation, which thus furthers the current understanding of the role of FUBP3 in cancer. - Source: PubMed
Publication date: 2026/07/07
Kong LingyuFu ChaoxuLi XuesongChen MingxinLiu XinqiZhou MinWang TongshuPiao Hongxin - Glioblastoma (GBM) is the most prevalent primary malignant tumor of the adult central nervous system, characterized by pronounced vascularity that facilitates tumor proliferation, invasion, and progression. Although anti-angiogenic therapy has emerged as a potential treatment strategy for GBM, currently available anti-angiogenic agents, such as bevacizumab targeting VEGF, have demonstrated limited efficacy in improving patient survival. This underscores the urgent need for novel therapeutic targets and strategies. In this study, we identified that the expression of maternally expressed gene 3 (MEG3), a tumor-suppressive long non-coding RNA (lncRNA), is negatively correlated with patient prognosis. Spatial transcriptomics sequencing and RT-qPCR analyses revealed that MEG3 is highly expressed in glioma stem cells (GSCs). In vitro tube formation assays further demonstrated that MEG3 in GSCs promotes angiogenesis in human brain microvascular endothelial cells (HBMECs). Transcriptome sequencing identified VGF nerve growth factor inducible (VGF), a secreted pro-angiogenic protein, as a downstream target, and showed that MEG3 regulates the pro-angiogenic activity of GSCs by modulating VGF expression. RNA pull-down assays revealed that MEG3 binds to far upstream element-binding protein 1 (FUBP3), which also regulates VGF expression. In vivo, knockdown of MEG3 significantly extended survival in orthotopic xenograft models of GSCs. Immunohistochemical analysis of mouse tumor tissues showed a corresponding reduction in VGF levels and microvessel density following MEG3 knockdown. In conclusion, this study demonstrates that MEG3 in GSCs promotes GBM angiogenesis through a FUBP3-dependent induction of VGF expression, highlighting MEG3 as a potential therapeutic target for anti-angiogenic intervention in GBM. - Source: PubMed
Publication date: 2026/03/23
Li YuanLi YujieTang JiaxinKong XueSun SibaiWang WeiWu Haibo - BACKGROUND: Remission from pre-diabetes and type 2 diabetes (T2D) is frequently observed immediately after a duodenal/jejunal bypass. This demonstrates the reversibility of T2D and involvement of the proximal small intestine in T2D pathology. This study investigates the role of the duodenum in the pathophysiology of T2D, in line with the hypothesis, that exclusion of duodenum/jejunum in T2D (for example, in RYGB surgery) prevents release of unidentified factors that impair insulin sensitivity, leading to T2D remission. The study aimed at identifying novel protein therapeutic targets in human duodenum in T2D and clarifying aetiology. METHODS: Proteome analysis using nano LC-MS/MS was performed on human duodenum surgical samples: T2D (n = 9), pre-diabetics (n = 6) and non-diabetics (n = 11). Proteins were quantified and analysed using MaxQuant and Perseus software. Linear discriminant (LDA), repeated k-fold cross-validation and receiver operating characteristic (ROC) analyses were used to segregate disease groups for the highest-ranking proteins. Pilot mRNA expression of five selected protein targets was analysed using real-time RT-qPCR on duodenum from human and the pre-clinical high-fat diet C57BL/6J mouse model of pre-diabetes. RESULTS: Proteomics identified and quantified significant changes in 23 proteins (one-way-ANOVA and Holm adjusted pairwise comparisons), differentiating pre-diabetes and T2D. LDA analyses accurately distinguished disease states and identified highest ranking for 10 proteins distinguishing type 2 diabetics, pre-diabetics and non-diabetics with first linear discriminant LD1 explaining 92% of differences; of which three proteins increased in pre-diabetes (DYNC1LI1, KIF5B and MAPRE1; ROC AUC = 0.89,0.82 and 0.86) are involved in vesicle and organelle transport along microtubules to and from the periphery; and seven proteins decrease in T2D (FUBP3, TPPP, NDUFAB1, ATP2B4, NPLOC4, DHRS4, CHMP3; ROC AUC = 0.81, 0.81, 0.77, 0.83, 0.82, 0.83, 0.76) revealing disruption in gene transcription, microtubule stability, mitochondrial function, Ca2+ signalling, unfolded protein response, redox status and multivesicular body formation. Two secreted proteins (APOA4 and RBP4; ROC AUC = 0.79 and 0.80) were also increased in T2D. Modelling using k-fold cross-validation, identified predictive power for 17 of the 23 proteins. At the mRNA level only borderline significant changes in Chmp3 and Fubp3 were detected using the duodenum of the pre-clinical high-fat diet C57BL/6J mouse model of pre-diabetes. CONCLUSION: Overall, this study addresses a critical knowledge gap, supports our hypothesis, and contributes to a deeper understanding of intestinal involvement in T2D pathogenesis, by examining how changes in the duodenum proteome landscape might reveal mechanisms that contribute to metabolic imbalance in T2D. While these results are currently purely cross-sectional and associative, and their contribution to causality and pathophysiological interpretation for T2D remain to be determined, they expand the frontiers of research on gut-targeted therapies in T2D, and lay groundwork for future translational research into gut-centred drug development to treat T2D or achieve controlled prevention or medical remission of T2D. - Source: PubMed
Publication date: 2026/03/16
Alves Beatriz D GMonteiro PaulaMartins Pedro CBraga JoséMatthiesen RuneVideira José Flávio GMollet Inês G - The Duroc × (Landrace × Yorkshire) (DLY) pig is a cornerstone of three-way crossbreeding system. Nevertheless, advances in commercial crossbred performance have been constrained by the dearth of high-resolution genomic resources for this key population. Here, we report the sequencing and assembly of 16 haplotype-resolved, chromosome-level genome assemblies derived from eight DLY pigs. These assemblies exhibited high continuity (contig N50: 18.17-29.54 Mb) and completeness (BUSCO: 99.3-99.4%), with sequences successfully localized to the 19 chromosomes. Genome annotation revealed an average of 21,922 protein-coding genes and 44.66% repetitive sequences per assembly. Comparative genomic analysis against the current reference genome Sscrofa11.1 enabled the construction of a non-redundant SV catalog comprising 130,416 variants, nearly half of which (48.99%) were novel relative to existing pig pan-genome SV panel. These SVs clustered non-randomly into 231 "SV hotspots" that were significantly enriched in protein-coding genes and putative regulatory elements. Functional analyses further linked these SV hotspots to quantitative trait loci (QTLs) associated with economically important traits. A focused analysis of a 3.43 Mb hotspot on chromosome 1, overlapping a known QTL for average daily gain, revealed eight high-frequency SVs in open chromatin regions near candidate genes (, , , , and ), suggesting a cis-regulatory mechanism that may influence gene expression. Collectively, this work provides the first haplotype-resolved genomic resource for commercial crossbred pigs, and establishes a foundational framework for deciphering the genomic architecture of hybrid vigor and advancing precision breeding in swine. - Source: PubMed
Publication date: 2026/01/31
Wen JiaolongQiu HaiqiDeng ShaoxiongWang ShiyuanLiu YiyiLin MengYang JieWu ZhenfangLiu LangqingQiu Yibin - Vascular invasion is associated with metastasis and poor prognosis in patients with lung adenocarcinoma (LUAD). Recent studies have highlighted the role of intercellular mitochondrial transfer, mediated by both contact-dependent and contact-independent mechanisms, in tumor progression. Here, we reveal an abnormal accumulation of mitochondria in vascular endothelial cells invaded by tumor cells. Further in vivo and in vitro experiments demonstrated that tumor cells can transfer mitochondria with highly expressed mitochondrial tRNA-derived small RNAs (tsRNAs), mt-5'tiRNA-34-GlnTTG, to endothelial cells. Mechanistic investigations indicated that mt-5'tiRNA-34-GlnTTG binds to FUBP3 and facilitates its translocation, ultimately enhancing ribosomal assembly efficiency and translation rates in endothelial cells. This molecular cascade leads to increased endothelial cell proliferation and migration, thereby promoting LUAD metastasis. Moreover, we demonstrated the potential clinical translational value of lipid nanoparticles(LNPs) encapsulating mt-5'tiRNA-34-GlnTTG inhibitors in animal experiments. Utilizing LNPs encapsulating mt-5'tiRNA-34-GlnTTG inhibitors effectively suppressed lung cancer metastasis in in vivo models. These findings reveal a novel mechanism of LUAD progression mediated by mitochondrial tsRNA transfer and highlight a promising therapeutic strategy for limiting metastatic spread. - Source: PubMed
Publication date: 2026/02/17
Liang SiWang QinglinZhang MinhaoSong XumingZhang YijianWang HuiFeng YipengLi RutaoXia WenjieXu LinDong GaochaoMao QixingJiang Feng