FOXM1
- Known as:
- FOXM1
- Catalog number:
- NB100-74659
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- FOXM1
Related genes to: FOXM1
- 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
Related articles to: FOXM1
- Cutaneous melanoma is a highly aggressive malignancy characterized by marked biological heterogeneity and variable clinical outcomes. Reliable biomarkers for prognostic stratification and biological characterization remain limited. This study aimed to investigate the expression pattern, prognostic significance, immune associations, and functional relevance of Forkhead box M1 (FOXM1) in melanoma. - Source: PubMed
Publication date: 2026/07/21
Li ZhichenZhu ZhenpengZhao RuixueWang LuyingHuo Ran - Atherosclerosis (AS) is closely linked to endothelial cell (EC) senescence and mitochondrial dysfunction, which impair vascular repair. Resveratrol (RSV) has antioxidant, anti-inflammatory, and pro-angiogenic effects, but its clinical use is restricted by poor bioavailability. This study aimed to construct a platelet membrane-coated resveratrol nanosystem (PM@RSV NPs) and investigate its mechanism of action in delaying the progression of AS by activating FOXM1 to improve mitochondrial function, inhibit EC senescence, and promote vascular regeneration. PM@RSV NPs were prepared using a solvent evaporation method combined with membrane-coating technology, and gene expression profiles and key regulatory networks were analyzed through RNA sequencing (RNA-seq), gene set enrichment analysis (GSEA), and least absolute shrinkage and selection operator (LASSO) regression. In vitro, PM@RSV NPs enhanced mitochondrial membrane potential and ATP generation while decreasing ROS accumulation and the number of SA-β-Gal-positive cells, accompanied by FOXM1 upregulation in ECs. In vivo experiments demonstrated that PM@RSV NPs significantly reduced plaque area, improved mitochondrial function, decreased levels of senescence markers, and promoted vascular regeneration via FOXM1 regulation. In addition, PM@RSV NPs preferentially accumulated in ox-LDL-injured MAECs and AS lesion-associated vascular endothelium, mainly through platelet-membrane adhesion proteins such as GPV and P-selectin; their biosafety was evaluated by EC viability/apoptosis assays, histological examination of major organs, and serum biochemical indices of liver and kidney function. This study confirmed that PM@RSV NPs improved mitochondrial function, inhibited endothelial senescence, and enhanced vascular regeneration by activating FOXM1, offering a novel therapeutic strategy for treating AS. - Source: PubMed
Xiao LiZhan ZexinLiu PingQin Bing - This study investigated the role of LINC00839 in regulating anoikis in hepatocellular carcinoma (HCC) cells. Bioinformatic analysis using UALCAN and Sparkle databases revealed that LINC00839 is highly expressed in HCC tissues and is associated with poor patient prognosis. Functional experiments demonstrated that LINC00839 expression was significantly upregulated in an anoikis model, and its overexpression inhibited apoptosis in HCC cells. This was evidenced by decreased levels of pro-apoptotic proteins Caspase-3 and Bax and increased levels of the anti-apoptotic protein Bcl-2. Transcriptome sequencing and database predictions identified the transcription factor FOXM1 as a key downstream effector. Crucially, siRNA-mediated knockdown of FOXM1 reversed the anti-anoikis effect of LINC00839, confirming its essential role in this pathway. Furthermore, LINC00839 overexpression promoted HCC cell proliferation, migration, and invasion. The study concludes that LINC00839 promotes hepatocellular carcinoma progression by inhibiting anoikis through the upregulation of FOXM1, highlighting its potential as a novel therapeutic target. - Source: PubMed
Publication date: 2026/07/17
Lu XiaohangLi MinpengYu YuanPan MengWang YunyongHe JiaqianTan JinnaYin HuiLin HongshengLi Mingfen - Cervical cancer treatment faces challenges like limited efficacy, side effects, and high costs. Hence, unearthing feasible objectives targeting pathogeny is compulsory for the management of cervical cancer. Ubiquitin-specific peptidase 5 (USP5) acts as an oncogene in various cancers, but its role in cervical cancer continues vague. USP5 expression was assessed bioinformatically and experimentally. Studies involving gain and loss of function were performed in Hela and CaSki cells as well as in a xenograft mouse model. Assays included reverse transcription-quantitative polymerase chain reaction (RT-qPCR), cell counting kit-8 (CCK-8), clonogenesis, flow cytometry, western blot, co-immunoprecipitation (Co-IP), and immunohistochemistry. High USP5 expression predicted poor prognosis in cervical cancer patients. USP5 knockdown inhibited cell proliferation, glycolysis (reducing GLUT1, PGC-1α, HK, LDHA expression, glucose uptake, and lactate production), and induced apoptosis, while overexpression had opposite effects. USP5 stabilized FOXM1 via deubiquitination, which was crucial for USP5-mediated oncogenic effects. , USP5 silencing suppressed tumor growth and glycolytic gene expression. USP5 promoted cervical cancer progression by enhancing proliferation and glycolysis and suppressing apoptosis through deubiquitination and stabilization of FOXM1, identifying it as a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/15
Su LiliChen RanHe TingtingSu XiuzhenWu ChangyiWei Xing - The Forkhead box M1 (FoxM1) transcription factor is a well-established oncogenic driver, with its overexpression closely associated with tumor grade, aggressiveness and adverse clinico-pathological features across multiple cancer types. This has garnered considerable therapeutic interest in FoxM1 as a potential target. However, current FoxM1 inhibition strategies suffer from significant limitations or lack clinical validation. In the present study, we employed a structure based rational drug design approach to screen small molecule inhibitors targeting the FoxM1-DNA binding domain (FoxM1-DBD) using the NCI compound library. Selected lead compounds exhibited potent suppression of FoxM1 and its targets in CaSki cervical cancer cells, outperforming conventional FoxM1 inhibitors. Electrophoretic Mobility Shift Assay (EMSA) and tryptophan specific fluorescence analyses confirmed direct and specific interaction of the compounds with FoxM1, resulting in effective disruption of FoxM1-DNA binding. Functional characterization revealed that these inhibitors robustly induced apoptosis as evidenced by enhanced PARP and caspase-7 cleavage. Furthermore, the lead compounds demonstrated activity across multiple cancer cell types and markedly attenuated key malignant traits of cancer cells, including proliferation, anchorage-independent growth, migration and invasion. Importantly, FoxM1 knockdown significantly diminished the tumor suppressive effects of the lead compounds thereby affirming target specificity. Collectively, our findings identify novel and selective small molecule inhibitors of FoxM1 that effectively disrupt FoxM1-driven oncogenic programs, highlighting their strong potential to evolve into credible anti-cancer therapeutics. - Source: PubMed
Publication date: 2026/07/16
Cheema Pradeep SinghJaiswal NehaDey Sanjay KumarNandi DeeptashreeSahani NandiniKundu SumanNag Alo