Ask about this productRelated genes to: FOXM1 antibody
- 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
Related articles to: FOXM1 antibody
- Breast cancer continues to be a leading and aggressive cancer in women. Despite improvements in early treatment, challenges such as rapid tumor proliferation, metastasis, and drug resistance persist. This research examines how the deubiquitinase ubiquitin-specific protease 5 (USP5) maintains Forkhead box M1 (FOXM1) protein stability and its impact on the advancement of breast cancer. - Source: PubMed
Publication date: 2026/03/21
Wang XiaoyanChen TingtingWu SongsongWu Youyi - Hepatocyte proliferation restores liver mass after partial hepatectomy (PHx), but the metabolic cost of this process remains unclear. Single-nucleus transcriptomics of mouse liver 48 h after 70% PHx revealed that EGFR-FOXM1 signalling drives mitotic entry while simultaneously suppressing PPARα-ACSL1-mediated lipid catabolism. Consequently, triglycerides and free fatty acids accumulate in regenerating tissue. Activating PPARα with the agonist Wy-14643 released this metabolic brake, accelerated hepatocyte proliferation via HIF1α-FOXM1, and improved post-PHx recovery. These data identify lipid-metabolic reprogramming as an EGFR-dependent collateral effect that can be pharmacologically reversed to enhance liver regeneration in surgical patients, offering a readily translatable strategy to reduce post-operative liver failure and shorten hospital stay after major hepatectomy. - Source: PubMed
Publication date: 2026/04/22
Hu YueleiSong ShifeiWang RuilinAn NiDiao JinmeiChen YuguoLiu JuanLv Guoyue - Osteoarthritis (OA) is characterized by progressive cartilage degradation accompanied by limited intrinsic repair capacity. Stromal vascular fraction (SVF) transplantation has demonstrated potential for regenerating damaged joint tissue; however, the pathological microenvironment impairs SVF stemness, thereby limiting therapeutic efficacy. Herein, we developed a bioinspired hydrogel formed via the cross-linking of hyaluronic acid-grafted dopamine and a fibroblast growth factor 2-mimetic peptide-modified RADA16-I. This injectable hydrogel combined excellent gelation performance with multifunctionality, particularly in enhancing SVF proliferation and chondrogenic differentiation. The hydrogel activated forkhead box M1 (FOXM1) - mediated epigenetic reprogramming, enhancing DNA repair capacity and increasing chromatin accessibility at pluripotency loci. In a rat OA model, combined hydrogel and SVF transplantation significantly enhanced articular cartilage regeneration and ameliorated OA symptoms. This study provides preliminary evidence showing that a biomaterial-mediated epigenetic reprogramming strategy improves recovery in OA, highlighting the therapeutic potential of the novel hydrogel for stem cell-based regenerative medicine. - Source: PubMed
Publication date: 2026/04/20
Hou WaifangChen YongfengXiao LongyouQi WeiDu TianshuSun QiangXue BoruiZhao QingheXie PengfeiYe ZiHan FeiGuo LingliJiao YangZhang RanranJia HongHuang XiaoGuo JianweiWang PengWang HuayiWang YuanruiChen WenjingWu HainingHe LiuminZhang Dawei - Nasopharyngeal carcinoma (NPC) is a highly aggressive malignancy. Given conventional therapy limitations, exploring non-apoptotic pathways like ferroptosis is crucial. Tryptophan (Trp) metabolic reprogramming is a key mechanism by which NPC cells evade ferroptosis by maintaining redox homeostasis. In this study, we investigated the anti-NPC activity of rAnguillin, a novel recombinant peptide derived from Anguilla anguilla, and elucidated the molecular mechanisms by which it induces ferroptosis via the FOXM1/PABPC1L axis. rAnguillin (7009 Da) was prepared via prokaryotic expression, with its primary sequence verified by LC-MS/MS. Notably, rAnguillin significantly inhibited NPC cell proliferation (IC = 3.306 μM at 24 h) and suppressed xenograft tumor growth in vivo in a dose-dependent manner. Mechanistically, as validated by CETSA and site-directed mutagenesis, rAnguillin directly interacted with the transcription factor FOXM1, triggering its ubiquitin-proteasome-dependent degradation. The downregulation of FOXM1 inhibited the transcriptional activation of PABPC1L, subsequently leading to the inactivation of the JAK2-STAT1 signaling axis. This cascade significantly suppressed the expression of rate-limiting enzymes such as IDO1, thereby depleting the tryptophan metabolic flux and the antioxidant protective effects of its metabolite, 3-hydroxyanthranilic acid (3-HAA). Ultimately, this disruption of redox homeostasis triggered robust ferroptosis, as evidenced by TEM and inhibitor rescue experiments. Taken together, this study demonstrates that rAnguillin induces ferroptosis in NPC cells by targeting FOXM1 for degradation, which subsequently suppresses the FOXM1-PABPC1L-JAK2/STAT1-tryptophan metabolism axis. These findings provide a promising therapeutic strategy and a potent drug candidate for the treatment of NPC. - Source: PubMed
Publication date: 2026/04/13
Yuan QianhuiZhao YanZhou FuxinZhang YuebinJia XinyueYao JihongLv MeiWang JihongLv Li - Triple negative breast cancer (TNBC) is associated with poor prognosis and is mainly treated with chemotherapy-based regimens, often including carboplatin. Resistance to carboplatin is a common clinical issue that is either initially present or develops with treatment. Overcoming this resistance is a significant clinical challenge, which highlights the need for novel therapeutic strategies. We used a pooled shRNA screening approach with a chemoresistant TNBC patient-derived xenograft (PDX) cell (PDXC) line to identify targets whose knockdown would enhance the efficacy of carboplatin. This screening led to the identification of the ATR (ataxia telangiectasia and Rad3-related) gene as a key therapeutic vulnerability. Inhibiting ATR with BAY1895344 or AZD6738 re-sensitized carboplatin-resistant PDXCs and PDXs to carboplatin, resulting in an increase in DNA damage, and apoptosis. ATR inhibition prevents carboplatin-resistant cells from effectively engaging the S and G2/M checkpoints required for DNA repair, leading to mitotic catastrophe. We further identified that the addition of ATR inhibitors to carboplatin enabled FOXM1-targeted gene program leading to premature passage into mitosis. Moreover, targeting PKMYT1, a regulator of cyclin-dependent kinase 1 (CDK1) controlling the G2/M checkpoint, through knockdown or with the novel PKMYT1 inhibitor RP-6306, also enhanced carboplatin efficacy in our TNBC PDXC. Molecular factors associated with response to the ATR inhibitor/carboplatin combination included low RNA levels of PKMYT1. These results underscore the pivotal roles of ATR and PKMYT1 in mediating resistance to carboplatin in TNBC and support targeting these pathways to overcome carboplatin resistance in this disease. - Source: PubMed
Publication date: 2026/04/13
Guay JulietKuasne HellenChabot CatherineBozek KathrynMajedi YasaminBuchanan MargueriteAguilar-Mahecha AdrianaBareke EricUlmer BenjaminKong TimYang KangningLiao MinyanElebute OluwadaraGuo RuiningMonast AnieMorin GenevièveHuang SidongPark MoragBasik Mark