FOXM1 Blocking Peptide
- Known as:
- FOXM1 Blocking Peptide
- Catalog number:
- BP301-533
- Product Quantity:
- 50 ug
- Category:
- Peptides
- Supplier:
- Beth
- Gene target:
- FOXM1 Blocking Peptide
Related genes to: FOXM1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: FOXM1 Blocking Peptide
- Lysine β-hydroxybutyrylation (Kbhb) is a metabolite-derived post-translational modification of histone and non-histone proteins that couples β-hydroxybutyrate (BHB) availability to gene expression. Yet the transcription factors that govern the Kbhb substrate program in cancer remain unidentified. Existing studies have cataloged Kbhb-modified substrates or examined individual proteins, without identifying the transcriptional regulators of the program in a defined tumor context. Here, we performed network-based master regulator analysis (MRA), implemented in the viper package, on a molecular signature restricted to experimentally validated Kbhb substrates, across two independent PAM50 Basal-like breast cancer (BLBC) cohorts profiled on orthogonal platforms: TCGA-BRCA (RNA-seq; n = 195 tumor, 113 normal) and METABRIC (microarray; = 209 tumor, 148 normal). Dataset-specific regulatory networks were inferred with ARACNe-AP and integrated by cross-platform Stouffer meta-analysis. Of 1493 Kbhb substrates, 1322 and 1213 were expressed in the respective cohorts. The analysis identified seven concordant transcriptional master regulators (six activated, one repressed; cross-cohort NES correlation r = 0.64), with CENPA (meta-NES +4.55) and FOXM1 (meta-NES +4.27) as the dominant drivers. These findings nominate a BHB-Kbhb-FOXM1/CENPA axis linking ketone-body metabolism to mitotic transcription, with potentially protumoral implications for ketogenic regimens in BLBC. - Source: PubMed
Publication date: 2026/08/06
Tovar HugoHernández-Lemus Enrique - Estrogen receptor (ER)-positive breast cancer (BrCa) accounts for two-thirds of all BrCa cases worldwide. Therefore, ER-targeted endocrine therapy is the standard treatment for this disease. There has been a recent trend towards developing combination therapies using molecularly targeted drugs to improve outcomes. This study aimed to identify therapeutic targets demonstrating efficacy when combined with fulvestrant (a selective ER downregulator/degrader). We generated microRNA (miRNA) signatures from fulvestrant-treated MCF-7 cells by RNA sequencing. From the signature, we evaluated because its expression was elevated by fulvestrant treatment in MCF-7 cells. Also, in expression analysis by subtype of BrCa patients, expression was suppressed only in luminal BrCa. Ectopic expression assays revealed that attenuated the malignant phenotypes of MCF-7 cells. We searched for genes regulated by and discovered that 11 (, , , , , , , , , , and ) are closely involved in BrCa molecular pathogenesis. Among these target genes, we focused on (), a transcription factor regulating cell cycle progression and division. Notably, combination therapy with fulvestrant and a inhibitor significantly suppressed MCF-7 cell proliferation. From the miRNA signature established in this study, we identified antitumor and its target genes and used these findings to explore candidate drugs with potential efficacy when combined with fulvestrant. - Source: PubMed
Publication date: 2026/07/29
Nagata AyakoTomioka YuyaYasudome RyutaroToda HirokoTokunaga TakuyaNagata YukiKato MayukoShinden YoshiakiNakajo AkihiroSeki Naohiko - Acute myeloid leukemia (AML) remains a therapeutic challenge due to complex oncogenic networks, including the often-undruggable MYC pathway. Here, we present an integrated in silico framework combining transcriptomic analysis, machine learning, and molecular dynamics (MD) simulations to explore potential therapeutic approaches targeting vault RNA1-1 (VTRNA1-1) in AML. RNA-seq profiling revealed that VTRNA1-1 depletion is associated with a profound disruption of the MYC and FOXM1 regulatory axes. To highlight compounds capable of recapitulating this transcriptomic signature, we developed a machine learning pipeline utilizing a Random Forest classifier trained on a fully compiled L1000FWD database subset. Virtual screening of approved drugs predicted the anthelmintic niclosamide as a top candidate (98.17% mimic probability). Explainable AI further rationalized this prediction by highlighting specific fragments within niclosamide's salicylanilide core. Furthermore, a 200 ns MD simulation indicated favorable computational stability of niclosamide bound to the p62 (SQSTM1) ZZ domain. The complex showed rapid structural convergence (ligand RMSD plateauing at 1.65 nm) without dissociation, while maintaining strict receptor compactness (steady Radius of Gyration and solvent-accessible surface area) and a persistent interaction network of ~73 close atomic contacts. These findings suggest that niclosamide may function as a stable physical "lid" over the p62 ZZ domain, occluding its N-degron-binding cleft. Taken together, our computational framework highlights niclosamide as a promising candidate for AML drug repurposing, providing a hypothesis-generating foundation that warrants rigorous experimental validation. - Source: PubMed
Publication date: 2026/08/04
Hatayama YukiShimohiro HisashiKawamura Koji - Understanding adaptive evolution has long fascinated evolutionary biologists. Adaptive phenotypic divergence is often driven by modifications to protein-coding sequences. The group exhibits relatively lower echolocation frequencies relative to body size compared with other rhinolophids, implying distinct evolutionary trajectories. Transcriptomes bridge genotypes and phenotypes. Here, we sequenced brain, liver and cochlea transcriptomes from one individual per species representing five taxa of the group. We performed comparative transcriptomic analyses and detected signals of positive selection. Seven hearing-related genes (, , , , , and ) were under positive selection. Unexpectedly, we also identified five vision-associated positively selected genes (, , , and ) in taxa with relatively lower echolocation frequencies within the group, indicating selection on sensory genes. Furthermore, candidate positively selected genes were significantly enriched in metabolism-related GO terms such as catalytic and oxidoreductase activity. Our study offers valuable transcriptomic resources for unraveling adaptive genetic mechanisms in horseshoe bats. - Source: PubMed
Publication date: 2026/07/30
Zhang LinSun KepingDai WentaoLiu TongLi AoqiangFeng Jiang - Anti-CD38 monoclonal antibodies have substantially improved outcomes in multiple myeloma (MM). Although daratumumab and isatuximab target the same antigen, accumulating evidence indicates that they differ in epitope recognition, biological activity, and immunomodulatory properties, suggesting these agents may not be therapeutically interchangeable. This review summarizes the molecular and immunological mechanisms underlying their distinct antitumor effects and their implications for treatment selection. Isatuximab binds near the catalytic site of CD38, resulting in potent enzymatic inhibition, enhanced antibody internalization, FOXM1 suppression, and reactive oxygen species-mediated cytotoxicity, which may preferentially target MM cells harboring 1q21 amplification. In contrast, daratumumab exerts prominent Fc-dependent immune effects, including trogocytosis-mediated downregulation of CD38 and VLA-4, suppression of cell adhesion-mediated drug resistance, and modulation of the immune microenvironment, potentially enhancing subsequent T-cell-redirecting therapies. We further discuss the relevance of these mechanistic differences to measurable residual disease, extramedullary disease, and sequencing with BCMA- and GPRC5D-directed immunotherapies. Finally, we propose a biology-guided treatment-selection model integrating genomic alterations, tumor biology, and immune remodeling to support precision medicine for patients with MM. - Source: PubMed
Publication date: 2026/07/24
Kikuchi JiroYasui Hiroshi