FOXM1 antibody (PE-Cy3)
- Known as:
- FOXM1 (anti-) (PE-cynanin 3)
- Catalog number:
- orb129151
- Product Quantity:
- 100 ul
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- FOXM1 antibody (PE-Cy3)
Related genes to: FOXM1 antibody (PE-Cy3)
- 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 (PE-Cy3)
Related articles to: FOXM1 antibody (PE-Cy3)
- 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 FoxM1and 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 - Excision repair cross-complementation group 6-like (ERCC6L), also known as PICH, is a centromere-associated SNF2 family ATPase that functions as a DNA helicase essential for mitotic chromosome segregation. Emerging evidence has established its significant oncogenic role across a broad spectrum of human malignancies. This review synthesizes current knowledge on the expression landscape, oncogenic functions, molecular mechanisms, and clinical significance of ERCC6L in cancer. Pan-cancer analyses consistently demonstrate that ERCC6L is frequently overexpressed in most tumor types compared to normal tissues, driven by mechanisms such as DNA amplification and promoter hypomethylation. This upregulation strongly correlates with aggressive clinicopathological features, including advanced tumor stage, metastasis, and poor patient prognosis across cancers like breast cancer, hepatocellular carcinoma, lung adenocarcinoma, and gastric cancer. Functionally, ERCC6L acts as a potent driver of malignant phenotypes by promoting uncontrolled proliferation through cell cycle acceleration, exerting anti-apoptotic effects, and enhancing invasion and metastasis via epithelial-mesenchymal transition. Mechanistically, ERCC6L operates at the nexus of multiple cancer pathways. It interacts with key mitotic regulators including PLK1, FOXM1, and KIF4A to govern cell cycle progression, activates pro-survival signaling cascades such as PI3K/AKT and NF-κB, and drives metastasis via PJA2-mediated p53 ubiquitination in lung adenocarcinoma. Furthermore, ERCC6L promotes metabolic reprogramming by stabilizing HIF-1α or transactivating PLK1 to drive aerobic glycolysis, and modulates DNA damage response, linking it to radio- and chemoresistance. Emerging evidence also connects ERCC6L to an immunosuppressive tumor microenvironment, with associations including Th2 cell infiltration, macrophage polarization, and reduced immune infiltration in HRD-high tumors, suggesting potential as a predictive biomarker for immunotherapy. The consistent association with aggressive tumor behavior positions ERCC6L as a valuable prognostic biomarker and a promising therapeutic target. Preclinical studies demonstrate that ERCC6L inhibition suppresses tumor growth and enhances treatment efficacy; however, current evidence is limited to and xenograft models, and substantial further validation is required before clinical translation. - Source: PubMed
Publication date: 2026/07/01
Jiang LingyuZhou HuaihaiHe JingQin JunqiHuang JianweiWei JiapingZhou YifanZhong Yonglong - Cardiomyocyte hyperplasia is the primary form of fetal heart growth, whereas this proliferative capacity is largely lost in adults across most mammalian species. The limited ability of adult cardiomyocytes to re-enter the cell cycle is a major cause of cardiac injury-induced morbidity and mortality. Here, we report that post-prandial Burmese python cardiomyocytes activate cell cycle re-entry to promote persistent cardiac growth. Burmese pythons normally eat large meals infrequently, resulting in reversible cardiomyocyte hypertrophy. We found that frequent feeding of large meals amplifies the modest post-prandial cardiac proliferation identified in an infrequent feeding interval. By activating E2F and Forkhead Box M1 (FoxM1) pro-proliferation transcriptional networks, frequently fed Burmese pythons potentiate cardiomyocyte proliferation in addition to transient cardiac myocyte hypertrophy. These findings identify hyperplasia as a natural means of sustained cardiac growth in Burmese pythons and demonstrate the use of pythons as a model for investigating non-injury induced proliferative cardiac remodeling. - Source: PubMed
Publication date: 2026/07/14
Tan YuxiaoMartin Thomas GPeter Angela KOzeroff Christopher DEbmeier Christopher CDoptis RyanHarrison BrookeLeinwand Leslie A