Ask about this productRelated 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
- Cisplatin resistance remains a major challenge in ovarian cancer, limiting treatment efficacy and reducing patient survival. While FOXM1 and calcium (Ca signaling have been individually implicated in chemoresistance, how transcriptional regulation is linked to Ca-dependent survival signaling remains poorly understood. To address this gap, we integrated bioinformatic analyses with functional and mechanistic studies in cisplatin-resistant (CR) ovarian cancer models. We found that FOXM1 transcriptionally activate STIM1, thereby enhancing store-operated Ca entry (SOCE) and sustaining cytosolic Ca levels. Elevated Ca influx-activated downstream interferon (IFN)/STAT1 signaling and increased expression of IFN-stimulated genes associated with DNA repair and anti-apoptotic programs. FOXM1 or STIM1 depletion and pharmacological SOCE inhibition attenuated STAT1 activation and restored cisplatin sensitivity, whereas STIM1 re-expression rescued the resistance phenotype following FOXM1 depletion. Using A2780/ACR and IGROV1/ICR ovarian cancer models, together with analyses of TCGA-OV and multiple GEO cohorts, we demonstrate that FOXM1 transcriptionally activates STIM1, thereby enhancing store-operated Ca entry and promoting STAT1-dependent IFN signaling. Genetic or pharmacological disruption of this pathway restored cisplatin sensitivity, identifying the FOXM1-STIM1/SOCE-STAT1 axis as a potential therapeutic vulnerability in platinum-resistant ovarian cancer. This study provides mechanistic insight into chemoresistance and highlights avenues for therapeutic intervention in patients with high FOXM1/STIM1 expression. - Source: PubMed
Publication date: 2026/09/15
Lin Tzu-ChienHsieh Meng-RuNguyen Hieu Dac HanhVisitsattapongse SarinpornChiu Wen-Tai - Breast cancer remains one of the leading causes of cancer-related mortality among women globally, underscoring the need for novel therapeutic targets. In this study, we identify Ubiquitin-Conjugating Enzyme E2 C (UBE2C) as a key regulator of tumor progression and therapeutic vulnerability in breast cancer. An integrated pan-cancer analysis reveals that UBE2C is significantly overexpressed in breast cancer and is associated with adverse clinical outcomes across various malignancies. Furthermore, single-cell analyses demonstrate that UBE2C enhances tumor proliferation through its regulation of cell cycle progression. Mechanistically, we establish Forkhead Box M1 (FOXM1) as the potential transcriptional regulator of UBE2C, evidenced by its specific binding to the UBE2C promoter and a conserved co-expression pattern across different cancers. Importantly, our findings predicted a synthetic lethal interaction between UBE2C and FOXM1, suggesting that concurrent inhibition of this pathway results in synergistic anticancer effects. This study identifies the FOXM1-UBE2C axis as a novel synthetic lethal pathway in breast cancer, offering potential as both a potential prognostic biomarker and a therapeutic target. - Source: PubMed
Publication date: 2026/10/02
Li WeiHuang GangSun YapingJiang Gaofeng - Clear cell renal cell carcinoma (ccRCC) is the most common histological subtype of renal cancer and remains associated with aggressive progression and poor clinical outcomes. Cartilage intermediate layer protein 2 (CILP2), an extracellular matrix-associated secreted protein, has been implicated in tumor-related processes, but its biological role and regulatory mechanism in ccRCC remain unclear. - Source: PubMed
Publication date: 2026/10/02
Sun JiajiaYan TongzhenZhang ZiyuanLiu HaoRen MeilingFan YidongGuo LiqiangYan KeqiangLiu Jikai - High-risk human papillomaviruses (HPVs) are the etiological agents of over 5% of cancers worldwide including those of the cervix and oropharynx. HPVs infect stratified epithelia and establish latent infections in basal cells but restrict productive replication or amplification to differentiated suprabasal cells. Despite the presence of viral genomes in most differentiated cells, only a subset of cells amplifies genomes as well as express late genes and these correspond to those that have re-entered G2/M, but the factors regulating this selectivity are unknown. To determine the signals that control the productive viral life cycle, single cell RNA seq was performed on cells that stably maintain high-risk HPV genomes following differentiation. Ten populations of undifferentiated and differentiating keratinocytes were identified, however, only one differentiated population had entered G2/M, expressed late genes and amplified viral genomes. One of the highly expressed replication factors in this population was the type II topoisomerase TOP2α while no other topoisomerases were similarly induced. TOP2α was found to bind to viral genomes, and acute depletion in differentiating cells blocked entry into G2/M, impaired genome amplification and abrogated late gene expression. Amplification also requires activation of DNA repair pathways through the induction of high levels of DNA breaks, and TOP2α accounted for more than half of the breaks present in differentiating cells. Increases in levels of TOP2α in differentiating cells were driven by the E7 oncoprotein acting through the transcription factor FOXM1, which also controls expression of G2/M factors suggesting an auto-regulatory loop. These studies identify TOP2α as a critical regulator of HPV genome amplification upon differentiation. - Source: PubMed
Publication date: 2026/09/24
Vats ArushiRozhok OlgaLaimins Laimonis - Mitogens trigger cell-cycle entry by activating E2F at the restriction point, which is followed by B-MYB/FOXM1 activation and progression to mitosis. How mitogens control continued cycling and cell-cycle exit after the restriction point is not well-understood. By developing an E2F and B-MYB/FOXM1 dual transcriptional biosensor system, we show that S/G2 phase duration is set by timed mitogen-regulated B-MYB/FOXM1 activation, while E2F activity gradually declines before mitosis. As a striking consequence, rapid B-MYB/FOXM1 activation shortens S/G2, delivering high mitotic E2F activity to daughter cells which keeps them cycling. Delayed B-MYB/FOXM1 activation prolongs S/G2, depleting mitotic E2F which drives daughters to quiescence. When S/G2 is further prolonged, partially activated B-MYB/FOXM1 frequently reverts, triggering mitotic bypass and polyploid quiescence. Thus, B-MYB/FOXM1 governs a tri-directional "G2 restriction point" where cells commit to continued cycling through early B-MYB/FOXM1 activation; cell-cycle exit through delayed B-MYB/FOXM1 activation; or mitotic bypass by B-MYB/FOXM1 inactivation. - Source: PubMed
Publication date: 2026/09/25
Rosenthal David LTsuruoka TatsukiKonagaya YumiGong BoGovindaraj VinodhiniUpadhya Samsara WRatnayeke NalinSaha DebaryaXia WenxinTeruel Mary NMeyer Tobias