FOXM1 antibody (Cy5.5)
- Known as:
- FOXM1 (anti-) (cynanin 5.5)
- Catalog number:
- orb123154
- Product Quantity:
- 100 ul
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- FOXM1 antibody (Cy5.5)
Related genes to: FOXM1 antibody (Cy5.5)
- 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 antibody (Cy5.5)
Related articles to: FOXM1 antibody (Cy5.5)
- Multiple cancers overexpress forkhead (FOX) box M1 (FOXM1), a transcription factor (TF) that holds great promise for developing cancer drugs. Herein, through yeast-two-hybrid (Y2H) screening, we obtained a novel FOXM1-targeting peptide M1-NP1, which significantly inhibited the cell cycle and migration of cancer cells. Mechanistically, M1-NP1 bound to the C-terminal region of FOXM1 and disrupted its interactions with the cell cycle-related kinase polo-like kinase 1 (PLK1) and the transcriptional co-activator cyclic adenosine monophosphate (AMP) response element-binding protein (CREB) binding protein (CBP), thus inhibiting FOXM1 transcriptional activities. Additionally, M1-NP1 affected FOXM1 distribution in cells, preventing FOXM1 from infiltrating the nucleus to exert its effects. Furthermore, M1-NP1 treatment in cancer cells downregulated the gene sets of cell cycle phase transition and upregulated the gene sets of cell adhesion. Moreover, M1-NP1's anti-cancer effects were confirmed in wild-type (WT) mice, without any notable toxic or side effects. In addition to its good safety indications, such as the low levels of immunogenicity and hemolysis, M1-NP1 also exhibited a favorable profile regarding stability and distribution in mice. Overall, M1-NP1 targets FOXM1 for cancer therapy. - Source: PubMed
Publication date: 2025/11/07
Pei ChaozhuXu ZiwuOuyang MinBu HuitongZou ZhenyuMa YutingZhu ZhengqingChen YanYu LiHuang MingminTan Yongjun - Cancer stem cells (CSCs) are a subpopulation with self-renewal and differentiation capacity that drive the progression, recurrence, and therapeutic resistance of patients with cervical cancer (CC). However, the complete set of genes that maintain stemness in CC remains incompletely defined. We aimed to identify key stemness-related genes and evaluate their prognostic utility, immune associations, and drug sensitivity. Through literature mining and CellMarker 2.0, we identified 1345 stemness-associated genes that overlapped with differentially expressed genes (DEGs) from the TCGA-CESC dataset (log2FC > 2, p < 0.05), yielding 216 stemness-related DEGs. A protein-protein interaction network (STRING) and CytoHubba (MCC algorithm) revealed ten hub genes (HGs): CCNB1, CCNA2, BUB1B, UBE2C, KIF11, CCNB2, KIF23, CDC20, CDC6, and FOXM1. Gene ontology and KEGG analyses revealed predominant enrichment in cell cycle progression. Cox regression and Kaplan‒Meier analyses identified BUB1B, CCNA2, CDC20, FOXM1, and KIF23 as risk factors for poor overall survival, with KIF11 emerging as an independent prognostic factor. HGs overexpression significantly correlated with altered infiltration of 15 immune cell types, including negative associations with CD8 + T and NK cells. We identified 661 unique drugs/chemicals targeting these HGs, including FDA-approved repurposed agents. Experimental validation via RT‒PCR confirmed significant overexpression of FOXM1 and KIF11 in CC tissues and cell lines compared with normal samples. These stemness-associated HGs, particularly FOXM1 and KIF11, may serve as potential prognostic biomarkers and therapeutic targets, warranting further investigation of stemness-driven CC progression. - Source: PubMed
Publication date: 2026/06/27
Kabekkodu Shama PrasadaRodrigues Alfa FlorenceHebbar PratheekshaBhat Samatha - A better understanding of the response of granulosa cells to exogenous hormone stimulation and how this impacts the complex interplay between the granulosa cells and the oocyte is crucial for the optimal management of infertile couples seeking IVF treatment. - Source: PubMed
Publication date: 2026/06/10
Medica AlexaKim Matthew EHung Wei-TingSohni AbhishekDuleba AntoniTan KunWilkinson Miles F - In the mammalian cerebellum, three types of astroglial cells-Bergmann glial cells (BGs), inner granule cell layer (IGL) astrocytes, and white matter (WM) astrocytes-arise in postnatal timing from two types of progenitors: Bergmann glia-like progenitors (BGLPs) and astrocyte-like progenitors (AsLPs). In contrast to AsLPs, which are commonly observed in other brain regions, BGLPs have not been well studied. Here, we investigate differentiation abilities, gene expression profiles and differentiation control mechanisms of BGLPs at postnatal stages. BGLPs and AsLPs decrease in number as development progresses from postnatal day 0 (P0), and are almost absent by P10. By utilizing an electroporation-based method to BGLPs, we found that P6 BGLPs differentiate into BGs and IGL astrocytes, but not into WM astrocytes, consistent with a previous report. However, P0 BGLPs were observed to differentiate into not only BGs and IGL astrocytes, but also WM astrocytes and a small number of molecular layer inhibitory neurons. By conducting spatial transcriptomic analysis with over 5000 probes (Xenium), we successfully identified distinct clusters corresponding to BGLPs at P0 and P6, respectively, and genes preferentially expressed in P0 and P6 BGLPs. In addition, upstream regulatory analysis using Enrichr identified Foxm1 and Nfia as candidate regulators that affect stage-specific properties of BGLPs. in vivo knockdown and overexpression experiments further demonstrated that precise regulation of Foxm1 and Nfia expression is important for proper progeny production from postnatal BGLPs. This study gives insights into understanding molecular nature and differentiation ability control of BGLPs during postnatal cerebellar development. - Source: PubMed
Suyama KyokaAdachi TomaMizuno MinamiJi KaiyuanIsogai ErikoHasegawa IkukoNishitani KayoSone MasakiMiyashita SatoshiOwa TomooHoshino Mikio - Therapy resistance remains a major obstacle to successful cancer treatment and is driven by complex interactions between tumor-intrinsic adaptive mechanisms and signals originating from the tumor microenvironment. Among the molecular regulators implicated in these processes, the transcription factor FOXM1 has emerged as a key mediator of DNA damage repair, cell cycle progression, and stress adaptation. Although FOXM1 has traditionally been studied as a regulator of intracellular signaling pathways, accumulating evidence suggests that its functions extend beyond canonical transcriptional control. In this review, we analyze current knowledge on the mechanisms regulating FOXM1 expression and activity and discuss how FOXM1 contributes to therapy resistance. We propose that FOXM1 should be viewed not merely as a regulator of individual oncogenic pathways but as a systems-level coordinator that integrates intracellular stress adaptation with microenvironment-driven resistance mechanisms. Particular attention is given to the FOXM1 interactome, complemented by an analysis of protein interaction data from BioGRID. We also discuss emerging evidence implicating FOXM1 in intercellular communication. To identify potential links between FOXM1 signaling and extracellular vesicle cargo, we analyzed the overlap between FOXM1 target genes and proteins identified in extracellular vesicle proteome databases. These emerging regulatory networks may represent previously underappreciated contributors to therapy resistance. - Source: PubMed
Publication date: 2026/06/10
Korolev Aleksei DBekbaeva Irina VShnaider Polina VShender Victoria O