Ask about this productRelated genes to: Fscn1 Blocking Peptide
- Gene:
- FSCN1 NIH gene
- Name:
- fascin actin-bundling protein 1
- Previous symbol:
- SNL
- Synonyms:
- p55, FLJ38511
- Chromosome:
- 7p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-16
- Date modifiied:
- 2016-10-05
Related products to: Fscn1 Blocking Peptide
Related articles to: Fscn1 Blocking Peptide
- circRNA is known to have regulatory functions across different cancers. Nevertheless, its regulatory functions in non-small cell lung cancer (NSCLC) are unknown. The present investigation aimed to research circ-FSCN1 expression in NSCLC cells and tissues employing high-throughput sequencing (HTS). NSCLC cells were investigated utilizing the CCK-8, EdU, and Transwell assays. Luciferase reporter assays were employed to verify circ-FSCN1 and its downstream target. Tumorigenesis and metastasis assays were performed to detect the role of circ-FSCN1 in NSCLC. Immunofluorescence was used to detect ROS deposition. The data indicated that the expression of hsa_circ_0004175 (circ-FSCN1) was elevated in NSCLC tissues and cells. The downregulation of circ-FSCN1 inhibited cellular migration and proliferation in the experiments. miR-506-3p downregulation or SLC7A1 overexpression reversed the suppression effects of sh-circ-FSCN1 on the proliferation and migration ability of H1299 and A549 cells. SLC7A1 overexpression reversed the inhibitory effects of miR-506-3p on the proliferation and migration ability of H1299 and A549 cells. The current investigation revealed that inhibiting miR-506-3p or overexpressing SLC7A1 reversed the enhancing effects of sh-circ-FSCN1 on ROS accumulation in H1299 and A549 cells. SLC7A1 overexpression reversed the enhancing effects of miR-506-3p on ROS accumulation in A549 and H1299 cells. Our investigation discovered that circ-FSCN1 affects ferroptosis and cell viability via the miR-506-3p/SLC7A1 pathway in NSCLC. circ-FSCN1 can function as a potential NSCLC diagnostic biomarker and therapy target. - Source: PubMed
Publication date: 2026/05/09
Yu WenxiLiu JiaoJin MingmingHuang GangHuang Qingqing - Mucinous colorectal adenocarcinoma (MAC) is characterized by poor prognosis and therapy resistance, yet its molecular and tumor microenvironment (TME) features remain inadequately understood, limiting the identification of effective therapeutic targets. Here, we performed a comprehensive analysis of MAC tumor characteristics and the TME using large-scale genetic and transcriptomic sequencing datasets. Our findings reveal that MAC tumor cells harbor a higher frequency of canonical mutations yet exhibit lower chromosomal instability. Additionally, we observed an increased infiltration of natural killer (NK) cells and highly expressed macrophages (Mac-SPP1) within the TME, along with heightened fibroblastic and myeloid inflammatory signals. Mac-SPP1, characterized by M2 macrophages, was associated with poor prognosis. Furthermore, we identified key prognosis-related genes, including , , and , and proposed potential therapeutic agents for overcoming treatment resistance. Our findings offer valuable insights into the molecular mechanisms underlying MAC and highlight the critical need for novel therapeutic strategies. - Source: PubMed
Publication date: 2026/03/30
Li JianxiaFu YangBai FanWu ZehuaQin GeDeng Yanhong - Base editors enable precise genome modification and have emerged as a promising therapeutic approach for correcting diseases caused by single-nucleotide variants. While the current efficient version of adenine base editors (ABEs), such as ABE8e, exhibits exceptional efficiency for A-to-G conversions, their clinical translation is hindered by persistent high off-target editing effects. Here, we applied artificial intelligence-assisted design a safe ABE variant, RDLot-ABE, with a narrow(4 nt) editing window and substantially lower DNA off-target editing activity compared to ABE8e. Moreover, targeted knockdown of Fscn1 for osteoarthritis treatment using RDLot-ABE alleviates cartilage degradation in explants derived from human patients. Notably, intra-articular delivery of the RDLot-ABE to reduce Fscn1 effectively arrests disease progression in a murine osteoarthritis model. These findings establish RDLot-ABE as a safe and precise tool, expanding the clinical potential of gene editing therapies. - Source: PubMed
Publication date: 2026/04/29
Yao JiaweiChen DalinZhang ZiyiRen JingxuanZhao ChengchengWang ShengfangShang MengyuJiang DaweiLi YinuoTang Su'anLi KaiZhang XiaohuiWang Xiaogang - - Source: PubMed
Publication date: 2026/04/24
Xu LingliJin ShanDong XingxingZhao XiaXu TongGuo YunmiaoTao LinPang Lijuan - 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