FGF_2
- Known as:
- FGF_2
- Catalog number:
- ANT-239
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- FGF_2
Related genes to: FGF_2
- Gene:
- FGF2 NIH gene
- Name:
- fibroblast growth factor 2
- Previous symbol:
- FGFB
- Synonyms:
- -
- Chromosome:
- 4q28.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- FGF13 NIH gene
- Name:
- fibroblast growth factor 13
- Previous symbol:
- -
- Synonyms:
- FHF2, FGF2
- Chromosome:
- Xq26.3-q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-16
- Date modifiied:
- 2018-02-13
- Gene:
- NUDT6 NIH gene
- Name:
- nudix hydrolase 6
- Previous symbol:
- -
- Synonyms:
- gfg-1, gfg, FGF2AS, FGF-AS
- Chromosome:
- 4q28.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-03
- Date modifiied:
- 2016-10-05
Related products to: FGF_2
Related articles to: FGF_2
- Myxofibrosarcoma (MFS) is a rare soft-tissue sarcoma with limited systemic therapy options, necessitating preclinical platforms that better simulate clinical drug responses. We investigated how 2D monolayers versus 3D spheroids shape the baseline transcriptome and doxorubicin (DOX)-responsive programs across six patient-derived MFS cell lines. RNA sequencing revealed that 3D culture induces a distinct transcriptomic state characterized by the enrichment of microenvironment-associated stress programs, such as hypoxia, inflammatory/NF-κB signaling, and glycolysis, alongside the suppression of proliferation-related pathways. Although the global DOX-induced transcriptional response was highly environment-dependent, we identified a robust core of six regulators-MCRIP1, FGF12, HGF, EMSY, FZD2, and SECISBP2-whose transcriptional changes consistently correlated with cell survival rates across both 2D and 3D geometries. These genes are involved in transcriptional plasticity, redox homeostasis, and bypass survival signaling, providing a mechanistic basis for DOX resistance that transcends culture conditions. Our findings demonstrate that while culture geometry is a critical determinant of the MFS transcriptome, a robust set of environment-agnostic regulators dictates DOX efficacy. Integrating 3D systems with these specific transcriptomic readouts enhances the interpretability of drug screenings and supports the prioritization of rational therapeutic combinations for this rare sarcoma. - Source: PubMed
Publication date: 2026/04/21
Yoshimatsu YukiShiota YomogiKondo Tadashi - The poor prognosis of lung adenocarcinoma (LUAD) remains unimproved. This study aimed to identify lymph node metastasis (LNM)-related and cellular immunity-related prognostic genes in LUAD and propose novel strategies to improve its prognosis. LUAD-related datasets were obtained from public databases. Prognostic genes and a prognostic model were obtained through various bioinformatics analyzes, and the immunotherapy response in risk groups was assessed. Subsequently, the expression levels of prognostic genes and the intercellular communication relationships were explored at the single-cell level. Moreover, malignant cells were identified, and their differentiation mechanisms were explored via inferCNV analysis. Additionally, FURIN was silenced and overexpressed to investigate its effects on the invasion, metastasis, and lymphangiogenesis of LUAD cells in vitro. RGS20, KYNU, RAET1E, FGF12, GJB2, CACNA2D2, FURIN, and GDF10 were identified as prognostic genes with LNM. In 4 datasets, LUAD patients with the high LNM and immune cell-related risk scores exhibited higher mortality rates compared to those in the low-risk group. Furthermore, individuals in the low-risk group demonstrated a greater propensity to derive advantages from immunotherapeutic interventions. Epithelial cells were identified as key cells, with CACNA2D2 being significantly up-regulated during their late-stage differentiation. Basal cells, the malignant subset within epithelial cells, showed elevated FURIN expression in the pre-differentiation phase, which declined in the middle and late phases. Functionally, FURIN was found to enhance the migratory and proliferative capacities of LUAD cells. Moreover, we demonstrated that FURIN accelerated lymphatic metastasis and lymphangiogenesis in vitro. In this paper, we identified LUAD prognostic genes with LNM and immune cell signatures, emphasized treating LUAD patients according to LNM- and immune cell-related risk scores, and provided novel ideas on how to improve poor prognosis and develop targeted therapy for LUAD. - Source: PubMed
Lin ChuanChen XuanSun YongTang XiaomeiJiang Yi - Hypertrophic cardiomyopathy (HCM) arises from genetic mutations in sarcomere proteins, resulting in major structural abnormalities and limited treatment options. Patients with HCM had reduced expression of the FGF12 (fibroblast growth factor 12), but its precise functional role remains unclear. - Source: PubMed
Publication date: 2026/04/14
Zhang TaojunYin KunlunLi TianjiaoWang ShuiyunZhou Zhou - After hind limb amputation in lizards, scars or short outgrowths are formed. FGFs may stimulate regeneration. Injections of FGF-1/-2 into the limb stump were made until 26 days post-amputation. This treatment gives rise to outgrowths of 1.5-3.5 mm within 40-70 days post-amputation, containing axial cartilages continuous with stump bones but missing muscles. Immunohistochemical localization in the outgrowth shows 5BrdU-labeled proliferating cells in the apical wound epidermis and perichondrium at 40-50 days post-amputation. Low to no proliferation is present in the axial cartilages and connective tissues at 60 and 70 days when growth terminates, except in scales. Immunodetection of FGF8 and Shh shows that the proteins are present at 30-40 days in the wound epidermis, apical connective tissue and perichondrium. These proteins lower to disappear in outgrowths from 50 to 70 days post-amputation, coincident with lowering of cell proliferation. The study suggests that the injection of FGF1/2 initially stimulates the growth of the limb mainly in cartilaginous axial structures, dense connective tissue, and new scales. No stimulation of muscle tissues is observed. Short cartilaginous rods of tibia, fibula or femur are produced but no autopodial elements. The presence of FGF8 and Shh in the wound epidermis and perichondrium of the initial outgrowths and their subsequent downfall reflect the initial growth and the later growth cessation. In future experiments, longer treatments with FGFs, hyaluronate and other signaling proteins, micro-injected in specific regions of the outgrowths may further enhance limb growth in this or other amniote models of limb regeneration. - Source: PubMed
Publication date: 2026/03/18
Alibardi Lorenzo - Fibroblast growth factor 12 (FGF12), a member of the intracellular fibroblast growth factor homologous factor (iFGF) subfamily, has been widely studied for its role in the modulation of voltage-gated ion channels. However, recent studies suggest that FGF12 possesses various cellular functions beyond ion channel regulation, particularly in cancer progression. Accumulating evidence indicates that the upregulation of FGF12 is associated with tumor survival, therapeutic resistance, and poor prognosis through signaling pathways independent of its canonical ion channel interactions. This review summarizes the current understanding of FGF12's non-canonical functions, highlights its emerging roles in cellular regulation, and discusses its potential mechanism in oncogenic progression. Understanding these novel functions may provide a new aspect for therapeutic targeting of FGF12 in malignancies. - Source: PubMed
Publication date: 2026/02/19
Huang ZechaoDong Xuesen