CDC25A Antibody
- Known as:
- CDC25A Antibody
- Catalog number:
- 32202
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CDC25A Antibody
Related genes to: CDC25A Antibody
- Gene:
- CDC25A NIH gene
- Name:
- cell division cycle 25A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-31
- Date modifiied:
- 2017-12-06
Related products to: CDC25A Antibody
Related articles to: CDC25A Antibody
- Various 2-fluorophenyl-adamantane analogs were studied to examine the potential for developing anticancer agents. This approach combined the synthesis of novel analogs spanning several structural variations, followed by in vitro cytotoxicity assessment, then computational studies utilizing network pharmacology, molecular docking, and density functional theory (DFT) techniques. 2-fluorophenyl-adamantanyl amides were synthesized by reacting a primary amine scaffold with the required acid chlorides. Anticancer activity was performed on PANC-1, DU145, A375, and MCF7 cells using a Sulforhodamine B colorimetric assay. IC50 values were determined to be as low as 0.53 µM for the most potent analog (AD-CA). Network pharmacology methods predicted biological targets including CDC25A enzyme. Molecular docking demonstrated binding within CDC25A. DFT calculations support the experimental findings by showing that AD-CA combines high nucleophilicity and electronic stability with a localized polar region around the chloroacetamide group. Molecular electrostatic potential and reduced density gradient (RDG) analyses further indicated favorable noncovalent interactions and limited steric congestion, consistent with its strong cytotoxic activity. Our findings suggest adamantane as a feasible backbone to develop anticancer agents which may act in-part via CDC25A interaction. - Source: PubMed
Publication date: 2026/09/16
Alamri MohammedRiadi YassineAlamri MubarakAbdel-Kader Maged - Premature ovarian failure (POF) is closely linked to ovarian granulosa cell (OGC) senescence and cell cycle arrest. This study explored the role of the miR-322/Klotho axis in OGC aging. Using a cyclophosphamide-induced mouse model and cultured OGCs, we found Klotho significantly downregulated in POF, inversely correlating with elevated miR-322 and senescence markers p16, p21, and p53. Luciferase assays confirmed Klotho as a direct miR-322 target. miR-322 overexpression induced G0/G1 and G2/M phase arrest and OGC senescence by silencing Klotho, while miR-322 inhibition partially rescued the POF phenotype. miR-322 knock-in mice exhibited reduced ovarian weight, increased follicular atresia, and altered E2/FSH levels, mimicking clinical POF. Mechanistically, the miR-322/Klotho axis modulated cell cycle regulators, upregulating CHK1 and downregulating CDC25A, CDK2, and Cyclin A/E. Thus, miR-322 promotes OGC senescence and POF by targeting Klotho to activate cell cycle inhibition pathways, identifying this axis as a critical epigenetic regulator of ovarian aging and a potential therapeutic target. - Source: PubMed
Publication date: 2026/09/09
Cui ZeyuLai YanchenChen XiangfengWang ChunxiaZhang BimengLiu Te - Oral squamous cell carcinoma (OSCC) is characterized by aggressive growth and frequent recurrence, highlighting the need for novel targeted therapies. Magnolol, a bioactive compound derived from , exhibits anti-tumor activity. In this study, we synthesized a methoxylated derivative, 2-O-methylmagnolol (MM1), and evaluated the anti-OSCC efficacy and underlying mechanisms of magnolol and MM1. - Source: PubMed
Publication date: 2026/07/01
Chen Chi-YuanShieh Tzong-MingChen Chin-ChuanLeu Yann-LiiChu Yu-DeLiou Miaw-JeneLiu Yi-TsenLin Hsin-WeiChen Kai-YinYu Cheng-ChiaWang Tong-Hong - Glioblastoma (GBM) is among the most aggressive primary brain tumors, marked by rapid proliferation, therapeutic resistance, and profound intratumoral heterogeneity. Epigenetic regulators such as lysine-specific demethylase 1A (KDM1A) and histone deacetylase 2 (HDAC2) are aberrantly expressed in resistant GBM subpopulations and strongly correlate with poor clinical outcomes. Here, we assessed the therapeutic potential of MPT0G521, a dual KDM1A/class I HDAC inhibitor, in disrupting epigenetic regulation and cell cycle progression. Bioinformatic analyses of resistance-associated gene profiles (temozolomide and 2 Gy radiation) and single-cell transcriptomic datasets from distinct tumor regions revealed enrichment of KDM1A and HDAC2 in high-cycling GBM clusters, particularly at invasive margins prone to recurrence. Functional assays demonstrated that MPT0G521 potently inhibited proliferation of both parental and temozolomide-resistant GBM cells, inducing G2/M arrest and apoptosis. Transcriptomic profiling further identified significant downregulation of centrosome integrity genes (FSD1, KIFC1), spindle regulators (TUBB, STMN1, KIF2C, KIF15), kinetochore components (AURKB, CDCA8, SPAG5), and G2/M checkpoint mediators (CENPF, MYBL2, CCNF, MYT1, CDC25A), resulting in disrupted mitotic progression. Mechanistically, MPT0G521 increased histone H3 methylation and acetylation, validating its dual inhibitory activity against KDM1A and class I HDACs. Collectively, these findings indicate that MPT0G521 disrupts the G2/M activation and mitotic machinery, thereby suppressing proliferative and resistant GBM subpopulations. This dual epigenetic strategy holds strong promise for overcoming GBM heterogeneity and reducing recurrence. - Source: PubMed
Publication date: 2026/09/02
Wu An-ChihChuang Jian-YingLiu Jr-JiunSalim Enrica AngelinaWu Ming-HsiaoJing Shih-WeiHsu Tsung-IChang Kwang-YuChang Wen-ChangThakur AmandeepLiou Jing-PingLo Wei-Lun - The review covers research on dual-target antitumor agents over the past five years. One of the targets is histone deacetylases (HDACs), while the second potential target is a protein group located both on the membrane surface (phosphatidylinositol 3-kinase (PI3K), anaplastic lymphoma kinase (ALK), receptor tyrosine kinase (AXL), tyrosine protein kinase (HER2), FMS-like tyrosine kinase (FLT3), and vascular endothelial growth factor receptor (VEGFR2)) and in the nucleus (serine/threonine protein kinase Wee1, DNA methyltransferase (DNMT), dual-specificity phosphatase (CDC25A), an enzyme from the cyclin-dependent kinase family (CDK9), dual-specificity tyrosine-serine/threonine kinase (DYRK2), and BET family proteins (BRD4, BD1, and BD2)). This review presents the results of studies on the inhibitory activity of various HDAC isoforms and other enzymes, as well as in vitro cytotoxicity studies on both neoplastic and healthy cells. It also includes selectivity studies, in vivo experiments (changes in tumor volume in mice) and oral bioavailability assessments. The review also describes the chemical structures of several dual-target agents and identifies the molecular fragments responsible for inhibiting different targets. Based on the studies reviewed in this paper, it can be concluded that some dual inhibitors have superior in vitro cytotoxicity and exhibit selectivity towards some tumor cells compared to monofunctional reference compounds. These findings may be useful for molecular design in the field of polypharmacology, with the aim of developing new dual-target molecules that exhibit improved antitumor activity and selectivity towards neoplastic cells. - Source: PubMed
Publication date: 2026/07/24
Yudaev PavelAleksandrova YuliaNeganova Margarita