FOXM1 (phospho)
- Known as:
- FOXM1 (phosphorilated)
- Catalog number:
- GTX14582
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- FOXM1 (phospho)
Related genes to: FOXM1 (phospho)
- 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: FOXM1 (phospho)
Related articles to: FOXM1 (phospho)
- The mTOR inhibitor everolimus improved progression-free survival in patients with hormone receptor-positive breast cancer resistant to hormone therapy. Despite initial success, everolimus has not yet realized its full therapeutic potential due to its associated toxicities and the development of resistance. Here, we exploited biocompatible lignin nanoparticles to enhance everolimus delivery and the mechanism of action in hormone receptor-positive breast cancer cells. Everolimus was released from the lignin nanoparticles in a concentration-dependent manner, following a Fickian diffusion-like model. The nanoparticles protected the drug from potential pH-induced degradation. Confocal microscopy confirmed the diffusion and cytoplasmic localization of lignin nanoparticles, as well as the efficient release of the drug. Everolimus release effectively inhibits the proliferation in breast cancer MCF7 cells. EVE/LNPs showed an improved in vitro antitumor effect compared to EVE against the MCF7 cell line (63 vs 81% survival rate at 10 nM). Under acidic pH conditions, the lignin nanoparticles underwent partial degradation, probably generating oligomers with potential modulating effects on mTOR and FOXM1. Molecular docking simulations showed that lignin oligomers could selectively interact with the ATP-binding cavity of mTOR. The affinity of these interactions was modulated by the redox state of the lignin oligomers, with the strongest bond being observed for quinone derivatives. This dual-action mechanism, which combines drug delivery and modulation of cellular signaling, offers a promising "on/off" switch approach to enhance everolimus-based cancer therapies. Further in vivo studies are warranted to validate these findings. - Source: PubMed
Publication date: 2026/02/23
Gabellone SofiaSpadazzi ChiaraPiccinino DavideCastrignanò TizianaCocchi ClaudiaCalabrese ChiaraCarotenuto GiovanniDe Vita AlessandroCeccotti Vlas NataliaMiserocchi GiacomoVanni SilviaDellavalle SofiaCani OnedaSbanchi GiuliaAvitabile DanieleLiverani ChiaraSaladino Raffaele - The Forkhead box M1 (FOXM1) transcription factor, recognized as a prominent oncogene, facilitates cell cycle progression and mitotic fidelity in aggressive cancers. Overexpression of FOXM1 is correlated with uncontrolled cell proliferation, metastasis, and poor prognosis. Despite its pivotal role in promoting genomic instability, cancer stemness, and metastasis, FOXM1 remains a clinically undruggable target. In this study, we identified masitinib mesylate, a small-molecule inhibitor known for its multitargeted tyrosine kinase inhibition, targeting c-Kit, PDGFRα, and PDGFRβ, as well as Lyn, which demonstrates anticancer activity in preclinical models. Masitinib mesylate emerges as a potent, novel first-in-class small-molecule inhibitor of FOXM1. prediction using pharmacophore-based virtual screening revealed that masitinib mesylate binds with high affinity to the FOXM1 DNA-binding domain (DBD) through hydrogen bonding with residues at His287 and Leu291, as well as a salt bridge with Asp293, effectively stabilizing the FOXM1-DNA interface and perturbing its activity. validation in the triple-negative breast cancer cell line MDA-MB-231 and the highly aggressive oral cancer cell line HSC-3 demonstrated that masitinib mesylate significantly reduces FOXM1 protein expression, thereby contributing to reduced cancer cell proliferation, stemness, and migration. Importantly, we validated these findings using human primary tumor slice cultures from patients with breast cancer and oral squamous cell cancer. Treatment with masitinib mesylate significantly induced apoptosis within the native tumor microenvironment, confirming its efficacy in heterogeneous, patient-derived tissues. Our findings establish a novel mechanistic link between masitinib mesylate and FOXM1 inhibition by DNA binding, providing a compelling rationale for drug repurposing, offering a targeted therapeutic strategy to disrupt the FOXM1-driven regulatory network in aggressive, therapy-resistant cancers. analyses predict a potential interaction of masitinib with the FOXM1 DNA-binding domain (DBD); however, further experimental validation is required to confirm direct binding. - Source: PubMed
Publication date: 2026/06/29
Gupta RajatSingh JaiShetty Shruti DayanandKumar Naveena A NKudva AdarshSrivastava Sandeep KumarChakrabarty Sanjiban - [...]. - Source: PubMed
Publication date: 2026/07/22
Oturkar Chetan CGandhi NishantRao PramodEng Kevin HMiller AustinSingh Prashant KZsiros EmeseOdunsi Kunle ODas Gokul M - Anaplastic thyroid carcinoma (ATC) is the most aggressive thyroid cancer type harboring TP53, TERT promoter and MAPK signaling alterations. Additionally, EZH2 overexpression leads to epigenetic silencing of tumor suppressor and cell differentiation genes. Here, we investigate the mechanism of EZH2 transcriptional activation in ATC. We used several luciferase reporter constructs with deletion of transcription factor (TF) binding sites identified in silico to determine EZH2 minimal promoter in ATC. MAPK signaling blockage with U0126, TF overexpression and knock-down strategies were used to evaluate EZH2 expression and reporter plasmid response, and the cross talk with TFs. As a result, we observed that EZH2 transcription is regulated by a minimal promoter of 107 bp (E3/4 region), that contains binding sites for TF NFYA, YY1 and FOXM1, highly expressed in ATC, that when deleted reduced EZH2 promoter activation. MAPK blockage reduced EZH2 and influenced YY1 and FOXM1 TF levels, while overexpression of NFYA, YY1 and FOXM1 resulted in pro-tumoral effects and EZH2 upregulation in papillary thyroid cancer cells. On the other hand, FOXM1 knock-down reduced EZH2 activation in ATC cells. Thus, we identified the minimal promoter region essential for EZH2 activation in ATC that is controlled by MAPK signaling in crosstalk with TFs. - Source: PubMed
Publication date: 2026/07/18
Cristovão Marcella Maringolode Mello Diego ClaroKimura Edna TerukoFuziwara Cesar Seigi - : Colorectal cancer (CRC) remains a heterogeneous disease, and improved biomarkers are needed to support prognostic assessment. This study aimed to characterize hub genes in CRC and evaluate whether a gene signature provides biologically meaningful and prognostic information in clinical-genomic models. : We integrated three GEO microarray datasets (GSE110223, GSE110224, and GSE23878) to identify common differentially expressed genes using adjusted p<0.05 and ∣log2FC∣>1. Hub genes and protein expression were identified through protein-protein interaction network analysis using maximal clique centrality and Human Protein Atlas, respectively. Prognostic relevance was evaluated in TCGA-COAD/READ using Kaplan-Meier analysis, multivariable Cox regression, Cox-derived prognostic indices, time-dependent ROC analysis, and regression-based machine learning for internal robustness. Principal component analysis (PCA) was used to derive a standardized PC1-based score from the 10-hub gene signature. : A ten-gene mitotic hub signature (TPX2, UBE2C, AURKA, NEK2, PRC1, CCNB1, CDK1, CEP55, FOXM1, and RRM2) was consistently upregulated across the three datasets and enriched for cell-cycle and mitotic pathways. Protein-level and survival analyses supported the biological relevance of several hub genes. In TCGA-COAD/READ, the signature showed limited standalone prognostic value and did not retain independent significance after adjustment for clinical variables, although it contributed modestly in integrated clinical-genomic models. PCA showed a one-dimensional signature, with PC1 capturing the dominant shared expression pattern. Gradient Boosting Regressor (R = 0.8035, MSE = 0.0473) supported the internal robustness of the DEG-based expression pattern. : The ten-gene mitotic hub signature represents a coherent CRC-related proliferative program with limited value as an isolated prognostic marker, but it may still be useful as part of integrated risk models that require external validation. - Source: PubMed
Publication date: 2026/07/08
Kamal EbtihalMoglad EhssanMohager Samah OAhmed MehadAldoseri Mobarak MahfodSuwayyid Barakat A AlBawadood Azizah SalimHamdan Hamdan ZAkbulut Mikail