TGT3 EMSA Probe Set
- Known as:
- TGT3 EMSA Probe Set
- Catalog number:
- AY1249P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- TGT3 EMSA Probe Set
Related genes to: TGT3 EMSA Probe Set
- Gene:
- FOXM1 NIH gene
- Name:
- forkhead box M1
- Previous symbol:
- FKHL16
- Synonyms:
- HFH-11, trident, HNF-3, INS-1, MPP2, MPHOSPH2, TGT3
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
Related products to: TGT3 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: TGT3 EMSA Probe Set
- Glioblastoma multiforme (GBM) is defined by rapid progression, high invasiveness, and a poor prognosis, with a median survival of only ≅13 months despite current treatments. Its marked genetic heterogeneity, high mutational burden, and cancer stem cell population make GBM exceptionally difficult to treat, highlighting the urgent need for more effective, multitargeted therapies. Non-coding RNAs, particularly tumor suppressor microRNAs (miRNAs), have gained attention for suppressing key oncogenic processes that drive tumorigenesis, metastasis, and drug resistance, positioning them as promising tools for targeting multiple oncogenic pathways. We recently found that FOXM1/AXL-eEF2K collaboratively drive GBM cell proliferation, survival, and invasion through the formation of a signaling hub complex. In this study, we employed miRNA prediction algorithms to identify a specific miRNA, in vitro functional assays and in vivo GBM flank model to target GBM tumorigenesis by distrupting the FOXM1/AXL-eEF2K signaling hub. Our results indicated that FOXM1, AXL, and eEF2K are overexpressed in GBM patient tumors. To target the FOXM1/AXL-eEF2K signaling hub, we identified miR-449b-5p, miR-329-3p, and miR-518c as potential co-inhibitors of FOXM1/AXL-eEF2K and suppressors of cell proliferation, migration-invasion, and spheroid formation. Furthermore, the combination of miR-449b-5p, miR-329-3p, and miR-518c treatments with temozolomide led to synergistic enhancements in cell proliferation suppression and the induction of apoptosis and ferroptosis. More importantly, in vivo miR-329-3p treatment led to remarkable suppression of GBM tumor xenografts. These findings indicate that miR-329-3p-based tumor suppressor therapy may offer a multitargeted approach for GBM treatment. - Source: PubMed
Publication date: 2026/05/04
Biltekin EzgiDilmac SayraKahraman NerminGul Ogun AliAkay Yasemin MWang ZhihuiAkay MetinOzpolat Bulent - Mantle cell lymphoma (MCL) is an aggressive B-cell non-Hodgkin lymphoma characterized by the cytogenetic abnormality and cyclin D1 overexpression. We have found evidence that Forkhead box M1 (FOXM1), a transcription factor with oncogenic potential, is important in the pathogenesis of MCL. Relatively high levels of FOXM1 proteins were detectable in all six MCL cell lines examined. By immunohistochemistry, we consistently found a subset of FOXM1-positive cells in MCL tumors. Analysis of two Gene Expression Omnibus (GEO) datasets from MCL patients showed that elevated levels significantly correlate with a worse clinical outcome. In MCL cell lines, inhibition of FOXM1 using thiostrepton or shRNA effectively triggered apoptosis and significantly reduced cell growth. FOXM1 forms a positive feedback loop with NFκB in MCL cells. Specifically, inhibition of FOXM1 dramatically decreased the protein level/transcription activity of p65, while enforced FOXM1 expression upregulated p65 and downregulated IκBα, a key NFκB inhibitor. Conversely, curcumin-mediated NFκB inhibition decreased the protein level/DNA binding of FOXM1, while transduction of a constitutively active IKKα construct into MCL cells significantly dampened the inhibitory effects of thiostrepton. Confocal microscopy revealed that FOXM1 and p65 colocalize with each other. In conclusion, FOXM1 and NFκB work collaboratively in promoting the growth and drug resistance of MCL, and FOXM1 may be a potentially useful therapeutic target. - Source: PubMed
Publication date: 2026/04/25
Zhang YujieSong YuqiAlmowaled MeaadShang ChuquanHua LeizhaoSandhu IrwindeepPeters AntheaChu Michael PWang PengLai Raymond - - Source: PubMed
Publication date: 2026/05/11
Kułaga DamianBosak NataliaPtaszkiewicz MagdaChrzan JuliaStaroń KatarzynaMarzec KamilaDrabczyk Anna KSiemieńska IzabelaKot MartaLatacz GniewomirKarnafał JoannaVelázquez-Martínez Carlos AMalarz KatarzynaMrozek-Wilczkiewicz AnnaBoguszewska-Czubara AnnaGreber KatarzynaCiura Krzesimir - This study aimed to elucidate the role of ROS-related genes in esophageal squamous cell carcinoma (ESCC) prognosis and the cellular mechanisms involving FOXM1 and SESN2. A prognostic model incorporating six genes (FOXM1, SESN2, APOD, GATM, HEBP2, STAT1) was developed using three ESCC gene expression datasets via univariate Cox regression, LASSO-Cox algorithm, and multivariate validation. Functional assays revealed that FOXM1 knockdown elevated intracellular ROS and malondialdehyde (MDA) levels while reducing total glutathione and antioxidant capacity, impairing proliferation, migration, and cell cycle progression. RNA-seq and luciferase assays confirmed SESN2 as a transcriptional target of FOXM1. Dual knockdown of FOXM1 and SESN2 exacerbated oxidative stress, decreased mitochondrial membrane potential, and increased cell death, accompanied by mitochondrial morphological changes (reduced shrinkage, increased membrane density). Western blotting showed decreased BCL2 and GPX4 expression but increased LC3-II and -mTOR levels. These findings demonstrate that the FOXM1-SESN2 axis shields ESCC cells from oxidative stress, offering a rationale for future mechanistic investigations. - Source: PubMed
Publication date: 2026/05/05
Wu ZhishengZhang XiaonaChen MantongGao ChenmengZheng XiaoqiPeng ZhongteDu ZepengWu Bingli - Liver fibrosis is not only a major cause of cirrhosis but also an important risk factor for hepatocellular carcinoma (HCC). Currently, few drugs can effectively reverse established liver fibrosis. FOXM1, a transcription factor aberrantly activated in chronic liver disease, has been implicated in fibrosis-associated hepatocarcinogenesis. Nevertheless, effective pharmacological strategies for targeting FOXM1 are still lacking. - Source: PubMed
Publication date: 2026/04/23
Wu DingyuDuan LeiTan DiHua XinyiLiang AnpingHuai RuipingQi ShanshanShang ZhixianJia ShijieQi HuiLiu XinrongZhao JielingJiang YuhongTan RuiMao Canquan