Ask about this productRelated genes to: FNDC3B antibody
- Gene:
- FNDC3B NIH gene
- Name:
- fibronectin type III domain containing 3B
- Previous symbol:
- -
- Synonyms:
- FAD104, DKFZp762K137, FLJ23399, PRO4979, YVTM2421
- Chromosome:
- 3q26.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-20
- Date modifiied:
- 2015-09-11
Related products to: FNDC3B antibody
Related articles to: FNDC3B antibody
- A tipping point signals the shift from a stable phase to a malignant state in cervical cancer progression. Identifying this transition is essential for early intervention, yet traditional biomarkers based on differential expression or undirected network measures often fail to capture it. Here, we introduce Causality-Directed Network Flow Entropy (CDNFE), a framework that quantifies entropy dynamics in directed regulatory networks to detect disease tipping points with superior sensitivity over expression-based methods. Applied to cervical cancer data which were derived from samples of different clinical stages collected from Luohe Central Hospital (single-cell, bulk transcriptome, simulations, and spatial transcriptomics), CDNFE consistently identified a precancerous tipping point and uncovered a biomarker module enriched for non-differentially expressed "dark genes." Within this module, FNDC3B and NECTIN4 emerged as central hubs, validated across multiple levels: (1) functionally essential in cervical cancer cell lines, (2) structurally important as driver nodes within regulatory networks, (3) mechanistically suggesting a potential link to PI3K/AKT signaling driven by epithelial-mesenchymal transition, and (4) spatially enriched in tumor regions in independent spatial transcriptomics sections. These findings establish CDNFE as a robust systems-level framework for tipping point detection and highlight FNDC3B and NECTIN4 as representative dark gene regulators of cervical cancer progression. - Source: PubMed
Publication date: 2026/04/24
Qiao RuiZhang QingweiSultan RabiaWang WeiZhang XinyanQu YizhenNa WangFu XiuhongJiao FengLi Peiluan - Accumulating evidence suggests reciprocal risk factors between periodontitis (PD) and systemic sclerosis (SSc). Ferroptosis, an iron-dependent and immune-related form of cell death, has been implicated in both diseases, yet its shared molecular mechanisms remain largely unclear. - Source: PubMed
Publication date: 2026/04/02
Zhang ShengchaoYang ShengweiGe CuiJi ChaoLin RuohanXue WenjuanLiu DongxiuChen Fulin - The microRNA (miR) cluster miR-143/145 represents a well-characterized tumor-suppressive regulatory system with a multifaceted role in prostate cancer. Both miRs are consistently downregulated during disease progression, and their loss is associated with enhanced proliferation, invasion, epithelial–mesenchymal transition, and metastatic competence. Mechanistically, the cluster modulates Rat Sarcoma Viral Oncogene Homolog (RAS)-Mitogen Activated Protein Kinase (MAPK) signaling via Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) and Extracellular Signal-Regulated Kinase 5 (ERK5), Tumor Protein p53 (p53)-dependent growth control through MYC Proto-Oncogene, Basic Helix-Loop-Helix Transcription Factor (c-MYC) repression, apoptosis via B-Cell Lymphoma 2 Interacting Protein 3 (BNIP3), and cytoskeleton-associated motility factors including Fascin Actin-Bundling Protein 1 (FSCN1), Human Enhancer of Filamentation 1/ Neural Precursor Cell Expressed, Developmentally Down-Regulated Protein 9 (HEF1/NEDD9), Golgi Membrane Protein 1 (GOLM1), and Fibronectin Type III Domain Containing 3B (FNDC3B). Downregulation is mainly driven by p53 dysfunction, promoter methylation, and RAS-dependent transcriptional repression. A defining feature is pronounced cell-type specificity, with tumor-suppressive effects in epithelial cells and context-dependent pro-angiogenic functions in stromal compartments, with direct translational relevance. Clinically, miR-143/145 contribute to multimarker diagnostic signatures, while reduced miR-145 correlates with adverse pathology and biochemical recurrence. Preclinical replacement strategies reduce tumor growth and enhance docetaxel sensitivity, yet context-dependent effects necessitate cell type-specific delivery. Overall, the cluster represents a central regulator with diagnostic, prognostic, and therapeutic potential requiring prospective validation. - Source: PubMed
Publication date: 2026/04/11
Stope Matthias BErb Holger H H - Circular RNA, usually produced through a back-splicing process, is a type of single-stranded RNA that is covalently bonded. Our research indicated that a spliceosome composed of SF3B4 and QKI promoted the back-splicing of FNDC3B, thereby promoting the generation of Circ-FNDC3B. Circ-FNDC3B is underexpressed in breast cancer and is characterized by a high metastatic risk. In addition, Circ-FNDC3B expression was reduced in breast cancer with larger tumor diameter, later clinical staging, and lymph node metastasis(LNM). The secondary structure of Circ-FNDC3B, specifically the 356-425 bp sequence, interacts with the biotin carboxylase domain of pyruvate carboxylase(PC), inhibiting the activity of PC. Low expression of Circ-FNDC3B enhances the activity of pyruvate carboxylase, thereby facilitating cell proliferation. The underlying mechanism involves the promotion of aspartate synthesis and the acceleration of the citrate - pyruvate cycle. This, in turn, promotes NADPH synthesis, thus alleviating the oxidative damage induced by reactive oxygen species (ROS). Furthermore, in human breast cancer organoids and a mouse model of lung metastasis, we have further validated that exogenous expression of circular RNA FNDC3B (Circ-FNDC3B) can inhibit the activity of pyruvate carboxylase (PC), thereby suppressing tumor proliferation and promoting tumor cell apoptosis. In general, upregulating the expression of circular Circ-FNDC3B can impede the progression of breast cancer. Implications: This study reveals significant heterogeneity of expression of circular RNAs commonly used to identify breast cancer metastasis, and confirms that circular RNAs affect the metabolic state of breast cancer through their binding proteins. - Source: PubMed
Publication date: 2026/03/16
Sen LiuHaiting LiuXiujie CuiXiangyu GuoShiming ChenRanran MaXing AiyanTiantian LiuYawen WangGao Peng - Both let-7a and miR-34a have been repeatedly studied as pivotal suppressors for Hepatocellular carcinoma; however, their combined regulations remain to be fully elucidated. In the present study, we performed a comprehensive in silico analysis for let-7a and miR-34a using a wealth of updated tools: miRWalk, Genetrail and miRnet. In addition, our study is the first to quantify both miRs and their three predicted yet not experimentally validated oncogenic targets: , and . This was assessed in HepG2 cell model following treatment by PEGP-vector expressing the miRs by MTT assay, florescence microscopy, qPCR and immune-florescence. Our bioinformatics analysis revealed a pool of common predicted hepatocarcinogenic targets shared by both let-7a and miR-34a. Importantly, three targets were identified as co-regulated through multiple canonical binding sites for each miR, and these had not been experimentally validated before. Furthermore, functional enrichment of these putative targets demonstrated their significant involvement in major and emerging HCC hallmarks, such as reprogramming of energy metabolism and evading immune destruction. These findings support our concept of simultaneous co-regulation of these oncogenes through the signaling networks and GO terms associated with both miRs. Consistently, our experimental results verified the significant overexpression of both miRs in HepG2 cells, leading to reduced tumor cell proliferation and decreased levels of the three oncogenic transcripts. Interestingly, miR-34a exhibited a superior suppression effect, reaching 38.7%, and was identified as the most significantly downregulated target at both transcriptional and translational levels. Our findings provide new insights into the interconnected anti-HCC effects of let-7a and miR-34a and highlight the potential of applying their combined use to achieve the best therapeutic outcomes for this invasive tumor. - Source: PubMed
Publication date: 2026/02/10
Soliman BanglyIbrahim Ahmed FawzySalem AhmedGhazy MohamedAbo-Elfadl Mahmoud TElHefnawi MahmoudFlores Mario