Ask about this productRelated genes to: FMN2 antibody
- Gene:
- FMN2 NIH gene
- Name:
- formin 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q43
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2018-11-15
Related products to: FMN2 antibody
Related articles to: FMN2 antibody
- Prostate cancer (PCa) progression to treatment-related neuroendocrine PCa (t-NEPC) often involves an early neuroendocrine differentiation (NED) phase lacking identified biomarkers. We utilized GeoMx Digital Spatial Profiling and single-cell RNA sequencing on human PCa tissues ranging from hormone-naïve (HNPC) to t-NEPC, with extensive multi-omics validation. Our results established early NED as a distinct, prognostically adverse subtype. We identified and validated 6 NED markers (FMN2, APLP1, SCG2, SCG3, CHGB, and RIMBP2), demonstrating specificity for NE cells and consistent upregulation throughout NEPC progression. Notably, the Hedgehog (Hh) pathway was specifically activated in early NED, manifested by high SHH ligand in neuroendocrine cells, GLI1 upregulation, and intercellular communication mediated via the SHH-Hh axis. Conversely, in late-stage t-NEPC, Hh pathway activity was significantly downregulated, while MYC-driven proliferation pathways predominated. A risk score derived from the 6-gene NED markers effectively stratified patients, correlating with pronounced NE features and shorter progression-free survival in 86 endocrine-treated patients and externally in The Cancer Genome Atlas (TCGA). In conclusion, this study delineates the dynamic molecular landscape of early NED, establishing a clinically promising biomarker panel and highlighting the Hh pathway as a stage-specific therapeutic target. - Source: PubMed
Publication date: 2026/05/06
Zhu WenhaoGao XiaomeiWang YinzhaoTang GuyuChen MinfengQi LinCai Yi - Mechanical force is a universal language of cells, yet which transcripts report tension on individual cytoskeletal polymers has remained unknown. Existing stretchers and drugs distort every filament simultaneously, blurring the signal. Here we apply a magnetogenetic approach, using antibody-guided 10 nm FeO nanoparticles to exert ∼0.5 pN force on β-actin, α-tubulin, or vimentin in human mesenchymal stem cells, and record the 20-h transcriptional response by bulk RNA-seq. Tension on microtubules amplifies Wnt, focal-adhesion, and extracellular-matrix modules; vimentin loading activates Hippo signalling, DNA-replication, and cell-cycle engines; actin loading elicits a TGF-β-centred oxidative-stress and ferroptosis programme, revealing a striking division of labour among the three polymers. Only four genes: KLHL24, RGS4, FMN2, and PDE4DIP are shared across the 384-405 differentially expressed transcripts per condition, exposing an orthogonal "filament code" for mechanosensation. The data overturn the view that the cytoskeleton transmits force through common pathways and identify a minimal, four-gene set that reports intracellular tension regardless of where it is applied. Because magnetic fields penetrate tissue centimetres deep and can be shaped in space and time, this platform offers a non-invasive route to steer stem-cell migration (via tubulin), proliferation (via vimentin), or cytoprotection (via actin), informing the design of mechano-responsive biomaterials and remotely controllable cell therapies. STATEMENT OF SIGNIFICANCE: Cells sense mechanical forces, but standard stretch devices and drugs activate the whole cytoskeleton at once, making it hard to isolate each filament's role. We used antibody-guided 10 nm FeO nanoparticles to apply ∼0.5 pN tension specifically to actin, microtubules, or vimentin in mesenchymal stem cells, then read out the 20 h response by RNA sequencing. Each filament triggers a largely distinct gene program, with only four shared genes, revealing a simple filament code for force signaling. This resolves a long-standing assignment problem and provides testable markers of intracellular tension. Because magnetic fields penetrate tissue and are easily shaped, our strategy suggests non-invasive ways to guide migration, proliferation, or cytoprotection, informing mechano-responsive biomaterials and remotely controllable cell therapies. - Source: PubMed
Publication date: 2026/02/11
Pozdina Varvara AKaravashkova Olga YPechnikova Nadezhda AMinin Artem SMaltseva Alexandra EDemin Alexander MAbakumov Maxim AYaremenko Alexey VZubarev Ilya V - Laying performance is a key metric for assessing avian reproductive efficiency. Ovarian tissues from Wanxi White Geese (WWGs) at different laying stages (birth period, laying period, and ceased period) were used in this study as research subjects. mRNA and circRNA expression profiles of ovarian tissues were constructed across various laying phases using transcriptome sequencing technology and bioinformatics approaches. The results revealed a total of 504 differentially expressed circRNAs (DEcircRNAs) (BO vs LO), 369 DEcircRNAs (LO vs CO), and 306 DEcircRNAs (BO vs CO) across different laying stages. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses demonstrated that DEcircRNA target genes were significantly enriched in processes including ovarian granulosa-cell proliferation, apoptosis, differentiation, and folliculogenesis. Concurrently, these targets were prominently implicated in phosphoinositide metabolism and played key roles in the GnRH, MAPK, and p53 signaling pathways. The expression of DEGs and proteins in ovarian tissues at different laying periods was detected by qRT-PCR technology and Western blot technology respectively. The results showed that the sequencing results were true and reliable. A ceRNA (circRNA-miRNA-mRNA) network was successfully constructed, and four key ceRNA regulatory axes implicated in ovarian development and steroid hormone synthesis/secretion were identified, namely novel_circ_107999-miR-1 44-y-NR2F2/TGM2, novel_circ_072697-miR-143-x-FMN2, novel_circ_031722-miR-101-x-CASP2/RPN 2, and novel_circ_100886-miR-101-y-PTX3/SEMA3 E/HSD3B1. The dual-luciferase reporter gene assay confirmed a targeting relationship between the novel_circ_072697-miR-143-x-FMN2 axis. In conclusion, this study system-atically explored the coordinated regulatory mechanisms of DEcircRNAs and their target genes, providing a theoretical foundation for identifying the key genes and molecular mechanisms underlying ovarian development in WWGs across different laying stages. These findings advance our understanding of the biological features of seasonal reproduction in this species and offer valuable insights for enhancing avian reproductive performance. - Source: PubMed
Publication date: 2026/01/22
Fan J HLi X JHou M MCai W WTong X WRen MJiang C SLi S H - Ovarian cancer (OC) remains a major threat to women's health, with chemoresistance driven by the immunosuppressive tumor microenvironment. Formin-2 (FMN2), a cytoskeletal regulator, was investigated for its role in OC chemoresistance and macrophage polarization. Bioinformatics analysis identified high FMN2 expression in chemotherapy-resistant OC cell lines, validated experimentally. Stable FMN2 knockdown cell lines were generated via lentiviral transfection. Functional assays revealed that FMN2 overexpression conferred chemoresistance in vitro and in vivo and promoted M2 macrophage polarization via the CCL2/JAK2/STAT3 pathway. Co-culture with M2 macrophages enhanced cisplatin (DDP) resistance in OC cells, mediated by CXCL1 secretion, which activated the epithelial-mesenchymal transition (EMT) pathway. Clinically, FMN2 levels correlated with CCL2 and CD206 (M2 marker) in platinum-resistant patients, and high FMN2, CCL2, or CD206 expression predicted poorer overall and disease-free survival. This study identifies FMN2 as a key mediator of chemoresistance and immune evasion in OC, proposing FMN2-CCL2-CD206 signaling and macrophage-derived CXCL1 as therapeutic targets and prognostic markers for chemotherapy response. - Source: PubMed
Publication date: 2025/12/20
Feng ShuoWang YapingRen RanWang XiaotongHan Lu - Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by oligo-anovulation, hyperandrogenism, and polycystic ovarian morphology. While its etiology is multifactorial, genetic susceptibility plays a key role in its pathophysiology. - Source: PubMed
Publication date: 2025/11/10
Ota KuniakiTakahashi ToshifumiNitta EmikoWatanabe KenjiIsayama KeishiroMorimoto YumikoTsuji KayoMatsuyama YukiyoMatsuyama TakehikoOta YoshiakiKanenishi KenjiMizukami YoichiShimoya Koichiro