FOXM1 antibody
- Known as:
- FOXM1 (anti-)
- Catalog number:
- orb135525
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- FOXM1 antibody
Related 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
- The ubiquitin signaling cascade plays a pivotal role in multiple cancer types, yet its role in melanoma progression remains incompletely elucidated. An unbiased and systematic analysis indicates that Ubiquitin-specific peptidase 10 (USP10), a member of USP gene family, was top priority prognostic signature for primary and metastatic melanoma progression-free survival and silencing USP10 markedly impairs the growth and metastatic potential of melanoma cells. We further uncover Forkhead box M1 (FOXM1) as a novel substrate of USP10. USP10 directly binds to FOXM1 and removes ubiquitin chains, thereby enhancing FOXM1 protein stability and driving melanoma progression. Notably, the lysine acetyltransferase KAT5 acetylates FOXM1 at residues K422 and K440, which strengthens the interaction between FOXM1 and USP10, facilitating deubiquitination and subsequent stabilization of FOXM1. Additionally, loss of either USP10 or FOXM1 suppresses the expression of the downstream target Telomerase reverse transcriptase (TERT), triggering cellular senescence. Importantly, we identify Golvatinib, as a novel inhibitor of USP10 that effectively curbs melanoma malignancy in both cellular and animal models. Taken together, these findings highlight the pro-tumorigenic role of USP10 in melanoma and suggest that disrupting the USP10/FOXM1 signaling axis could represent a viable therapeutic approach for treating this aggressive cancer. - Source: PubMed
Publication date: 2026/09/10
Qiu ZhiyuanSun ChenglianWang JuanLiang DapengWang ShangTian LiliDu TongdeHan Chuanchun - N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD) and its transformation product 6PPD-quinone (6PPDQ) are emerging tire-derived environmental contaminants, showing a potential tumor-promoting effect. However, their relevance to cutaneous squamous cell carcinoma (cSCC) remains unclear. Here, we used network toxicology and experimental validation to investigate their potential involvement in cSCC progression. A total of 91 candidate genes were identified, and enrichment analysis revealed their participation in oxidative stress response, epithelial proliferation, extracellular matrix degradation, and oncogenic pathways, including PI3K-Akt, MAPK, and IL-17 pathways. Machine learning identified six hub genes: , , , , , and . Immune profiling and single-cell RNA-sequencing analysis linked hub-gene expression patterns and tumor microenvironment features, with an emphasis on macrophages, T cells, and keratinocytes. Molecular docking prioritized MMP9 among the six candidate proteins, and molecular dynamics simulations characterized predicted MMP9-ligand complexes. Furthermore, 6PPDQ was found to promote cSCC cell proliferation and tumor growth in both in vitro and in vivo experiments. At the molecular level, 6PPDQ exposure was accompanied by increased PI3K p110α expression, elevated p-AKT/AKT ratio, and MMP9 upregulation, consistent with the computational predictions. Pharmacological AKT inhibition attenuated MMP9 upregulation and the 6PPDQ-associated growth response, while silencing reduced 6PPDQ-enhanced invasion and wound closure. Overall, this bioinformatics-led exploratory study suggests that 6PPDQ has tumor-promoting potential in experimental cSCC models and proposes PI3K-Akt/MMP9 activation as a preliminary mechanistic hypothesis. These findings provide candidate targets for future mechanistic and environmental risk studies. - Source: PubMed
Publication date: 2026/09/18
Song DekunChen YuluWu YueWu YuhaoChang LunhuiLiu XuanXu XiaoxiangYan GuorongZhang Guolong - USP5 is a deubiquitinating enzyme whose role in anti-PD-L1 resistance in breast cancer remains unclear. This study investigated whether USP5 contributes to resistance against the anti‑PD‑L1 antibody (atezolizumab) by regulating the FOXM1/Nectin2 axis. Anti-PD-L1-resistant and lung metastatic mouse models were established, combined with in vitro cellular assays, clinical sample analyses, and bioinformatics approaches. The results showed that USP5 was upregulated in breast cancer and stabilized FOXM1 via deubiquitination, which led to increased Nectin2 expression and resistance to CD8⁺ T cell-mediated killing. Knockdown of USP5 or its pharmacological inhibition with G9 synergized with anti-PD-L1 to suppress tumor growth, an effect that was reversible by Nectin2 overexpression. In conclusion, USP5 promotes breast cancer progression and anti-PD-L1 resistance by deubiquitinating FOXM1, thereby upregulating Nectin2 expression. Targeting USP5 enhances the efficacy of anti-PD-L1 therapy, offering a novel strategy to overcome immunotherapy resistance in breast cancer. - Source: PubMed
Publication date: 2026/09/22
Li GuangyanSu ZhiyuanZhang YutongDu QiguangXu ZhongkaiCui HeZhang Jianguo - Primitive hematopoietic stem cells (pHSCs) sustain lifelong hematopoiesis through tightly regulated transitions between quiescence and activation. Circadian oscillations influence hematopoiesis; however, the mechanisms coordinating metabolic state and stem cell function daily remain incompletely defined. Here, we show that circadian cues coordinated a program of mitochondrial remodeling, metabolic reprogramming, and structural adaptation in pHSCs. At night, peak melatonin levels were associated with reduced mitochondrial membrane potential, increased mitochondrial reactive oxygen species, and activation of DRP1 and PINK1 dependent mitophagy, resulting in enhanced long term repopulating capacity. In parallel, pHSCs exhibited increased glycolytic activity characterized by elevated glucose uptake, GLUT1 expression, AMPK phosphorylation, and HIF1α signaling. Mechanistically, mitochondrial remodeling was regulated in part by melatonin signaling, whereas glycolytic reprogramming was modulated by systemic circadian inputs, including feeding associated cues and Wnt/β-catenin signaling. FoxM1 and DRP1 contributed to mitochondrial quality control, while PGC1α dependent transcription supported compensatory mitochondrial biogenesis across the daily circadian cycle. These metabolic transitions were accompanied by dynamic changes in cell and nuclear size, linked to lamin A/C phosphorylation modulation. These coordinated processes defined a nocturnal state of enhanced stem cell fitness characterized by improved regenerative potential. Key features of glycolytic regulation were conserved in human HSCs, and in vitro melatonin treatment reduced the mitochondrial membrane potential and cell size of human pHSCs. Together, these findings establish a temporally regulated metabolic framework in which circadian cues partition mitochondrial and glycolytic programs to preserve stem cell maintenance and function, adding a new layer to pHSC metabolic physiology with clinical transplantation implications. - Source: PubMed
Publication date: 2026/09/21
Chakrabarti PriyasmitaSingh Abhishek KWilson Nicola KKucinski IwoKollet OritOrdonez Moreno Lizeth-AlejandraSimoni-Nieves ArturoVijayabaskar M SKinston Sarah JChang Tzu-HsuanWang Yi-HaoHaddad MontaserVaresi AngelicaPetrovich-Kopitman EkaterinaPorat ZivSmirnova TatianaPaulose JiffinChoudhuri AvikHogenesch JohnZhao You-YangHo Ping-ChihBuxboim AmnonZon Leonard IFilippi Marie-DominiqueMarkus Regina PDick John EXie Stephanie ZGottgens BertholdCancelas Jose ALapidot Tsvee - Advanced prostate cancer has increasingly developed a lethal neuroendocrine form, small cell/neuroendocrine prostate cancer (NEPC), as a consequence of the widespread use of highly potent androgen receptor signaling inhibitors in castration-resistant disease. The molecular mechanisms remain unclear and no effective therapies currently exist. We report that tryptophan hydroxylase 1 (TPH1), the enzyme responsible for peripheral serotonin biosynthesis - a neurotransmitter enriched in neuroendocrine tumors and a classical neuroendocrine biomarker - was upregulated in both de novo and therapy-induced human NEPC. TPH1 upregulation was necessary and sufficient for neuroendocrine differentiation and the NEPC phenotype through its enzymatic activity. Silencing TPH1 suppressed neuroendocrine plasticity and various aggressive behaviors of NEPC cells, including proliferation, invasion, sphere formation, and NEPC tumor xenograft growth. Mechanistically, TPH1 activated mTOR via intracellular serotonin-dependent serotonylation of mTOR at glutamine 2453, which triggered the induction of FOXM1 and E2F1 to drive NEPC differentiation and growth. Importantly, pharmacological inhibition of TPH1 using the clinically available inhibitor LX1606 effectively restricted growth and neuroendocrine marker expression in multiple NEPC cell lines and patient-derived xenografts. Collectively, these findings characterize TPH1's contribution to NEPC and suggest TPH1 as a potential therapeutic target. - Source: PubMed
Publication date: 2026/09/17
Wei JingWang JingChen JingruiZhang MichelleChen Chia-HuiPu TianjieO'Brien AliviaHargrove SephtisCorey EvaLin Tzu-PingGao Allen CWu Boyang Jason