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
- Patients with advanced malignant adrenal tumors face poor prognoses with limited treatment options. Emerging data suggest that these rare tumors exhibit immunogenicity, potentially benefiting from intensified immunotherapy. - Source: PubMed
Publication date: 2026/07/06
Schultheiß ChristophBesemer BrendaWillscher EdithPaschold LisaMersceman TifannyTalpin AliceSerger ClaraZippelius AlfredBerruti AlfredoGrisanti SalvatoreMenke-van der Houven van Oordt Catharina WillemienBaudin EricLandwehr Laura-SophieCapdevila JaumeSubbiah VivekGranberg DanGedske Daugaard KirstenTriebig AlexandraGauduchon ThibaultDo Cao ChristineGarcia Marie-EveMagalhaes JoaoChêne LaurentBinder Mascha - Forkhead box protein M1 (FOXM1) is a pivotal member of the forkhead box family of transcription factors, characterized by its marked overexpression in a wide range of human malignancies and its critical role in driving tumor progression through the regulation of cancer cell proliferation and invasion, making it an attractive target for anti-cancer therapy. However, comprehensive reviews detailing the role of FOXM1 in regulating tumor immunity are still lacking. In this review, we summarize the multiple roles of FOXM1 in regulating tumor immunity and assess its potential as a therapeutic target. FOXM1 plays a crucial role in regulating the tumor immune microenvironment by modulating immune checkpoints, influencing macrophage polarization, and affecting T cell differentiation and infiltration. Furthermore, FOXM1 also plays a regulatory role in key immune-related signaling pathways, including signal transducer and activator of transcription 1 (STAT1) and interferon stimulated gene (STING). Furthermore, the potential of targeting FOXM1 to enhance the efficacy of immunotherapies is discussed, with particular emphasis on overcoming challenges related to immune evasion, neurotoxicity, and therapeutic resistance. This review also summarizes the current landscape of FOXM1-targeted drug development and application, including small molecule inhibitors, peptide-based therapeutics, and combination treatment strategies, highlighting the promising clinical prospects of FOXM1 as a novel and multifaceted target in cancer therapy. - Source: PubMed
Publication date: 2026/07/06
Wang ShupingZhang KaifengYong TaoAn YuBai ShuangYuan ChangLiu HuayongLiu TiangeLi Zhipan - Esophageal Adenocarcinoma (EAC) is an aggressive malignancy with poor prognosis. The rising incidence of EAC in the past few decades underscores the need to better understand the molecular features of EAC. The role of the transcriptional co-factor Limb-Bud and Heart (LBH), implicated in embryonic development and Wnt signaling, remains unclearly characterized in gastrointestinal cancers. Given the importance of gastroesophageal reflux disease and acidic bile salts (ABS) exposure in EAC tumorigenesis and progression, we investigated the role of LBH in EAC carcinogenesis. - Source: PubMed
Publication date: 2026/07/02
Fo SydneeLu HengChen LeiPeng DunfaChen ZhengEl-Rifai WaelBallout Farah - 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