CDC25A Monoclonal Antibody [DCS120]
- Known as:
- CDC25A Monoclonal Antibody [DCS120]
- Catalog number:
- A-0460-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- CDC25A Monoclonal Antibody [DCS120]
Related genes to: CDC25A Monoclonal Antibody [DCS120]
- 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 Monoclonal Antibody [DCS120]
Related articles to: CDC25A Monoclonal Antibody [DCS120]
- Ferroptosis has been increasingly implicated in the progression of various tumors, including hepatocellular carcinoma (HCC). This study aimed to identify ferroptosis-related genes with prognostic significance in HCC. Differential expressed genes (DEGs) and long non-coding RNAs (DElncRNAs) were identified from TCGA LIHC RNA-seq data. A competitive endogenous RNA (ceRNA) network was established based on ferroptosis-related lncRNA-mRNA pairs. Prognostic genes were identified through survival analysis, and selected DEGs were further validated via quantitative PCR. Co-expression analysis identified 218 lncRNA-mRNA pairs, including 216 DEGs and 11 DElncRNAs. Among these, 11 upregulated ferroptosis-related genes were identified as predicted targets of the lncRNA DDX11-AS1. MiR-195 and miR-424 both regulated CDC25A and HELLS. Elevated expression of DDX11-AS1, CDC25A, EZH2, FANCD2, and HELLS was associated with poorer survival. In vitro cellular experiments showed that the knockdown of DDX11-AS1, CDC25A, and HELLS inhibited cell proliferation and invasion by promoting ferroptosis in Huh7 cells. The 11 ferroptosis-related genes and DDX11-AS1 may serve as valuable prognostic biomarkers and potential immunotherapeutic targets in HCC. - Source: PubMed
Publication date: 2026/06/25
Yan KaiHu FangfangTang HaodongZhou Jiahua - Phytochemicals showed potential application as anticancer agents. In the current investigation, quercetin, cold-pressed orange peel oil, and their mixture in their natural state and in micellar dispersion and nanoemulsions were examined for their activity to induce HCT116 and Caco-2 colorectal cancer cells to apoptosis. - Source: PubMed
Publication date: 2026/06/17
Abd-Rabou Ahmed AEdris Amr E - This work presents a novel, promising, and efficient strategy to develop potential Pt(IV) prodrugs for cancer chemotherapy while to simultaneously overcome the ″undruggability″ of CDC25A. New series of Pt(IV) complexes (-) bearing 1,4-naphthoquinone (NQ, a natural active skeleton) derivatives (-) as potential dual CDC25A/NF-κB inhibitory ligands were synthesized and characterized. Their in vitro and in vivo anticancer activities were subsequently evaluated. Mechanistic investigations revealed that , the most potent candidate with ligand , effectively depleted CDC25A levels in A2780 cancer cells through a synergistic effect mediated by DNA damage. Thus, triggered multimodal anticancer mechanisms, which included reactive oxygen species/endoplasmic reticulum stress-mediated mitochondrial apoptotic pathway, DNA damage coupled with S-phase cell cycle arrest, and autophagy-dependent ferroptosis. In A2780 xenograft models, administrated with a dosage of 8 mg/kg manifested superior tumor growth inhibition than both cisplatin and "cisplatin + " combination, along with satisfying low toxicity. - Source: PubMed
Publication date: 2026/06/11
Huang Yun-HouLiu YuanHu QinHuang YueLuo Sha-ShaLiu Rui-XueWen Chang-ChunLiu Yan-ChengStorr TimLiang Hong - Cullin-RING ligase 4 (CRL4) complexes achieve substrate specificity through DDB1-CUL4-associated factors (DCAFs), yet how individual DCAFs engage the adaptor protein DDB1 remains incompletely understood. Here, we report the cryo-electron microscopy structure of DCAF8 in complex with DDB1 (2.53 Å) and define the molecular determinants underlying CRL4 assembly and cell cycle progression. Our structure reveals that DCAF8 associates with DDB1 primarily through an N-terminal helix-loop-helix (HLH) motif that inserts into a conserved pocket formed by the BPA and BPC domains of DDB1. Disruption of this interface impairs complex assembly, attenuates CDC25A ubiquitination, and results in cell cycle defects. In contrast, residues within the conserved double DxR box of DCAF8 are positioned away from the DDB1 interface and are dispensable for adaptor binding. Together, these findings define a DCAF8-specific recruitment mechanism within CRL4 ubiquitin ligase assemblies. - Source: PubMed
Publication date: 2026/06/02
Shen MiaomiaoZhang HangChen MinYang JiaqiYuchi ZhiguangZhang HuaweiLiu Liren - Esophageal squamous cell carcinoma (ESCC) is aggressive with poor prognosis, frequently driven by chemotherapy resistance. Kinesin family member 18B (KIF18B) is implicated in tumor progression, but its role in ESCC chemoresistance remains unclear. To investigate KIF18B's clinical relevance and mechanistic contribution to oxaliplatin resistance in ESCC, KIF18B expression was analyzed in TCGA data, ESCC cell lines/tissues (qPCR, Western blot, IHC), and correlated with survival (Kaplan-Meier). Results showed that, KIF18B was significantly elevated in ESCC and correlated with shorter overall/progression-free survival. Knockdown reversed oxaliplatin resistance, reducing IC50 from 8.5 µM to 3 µM, restoring apoptosis, and inducing G2/M arrest. Silencing suppressed the ATR/CHK1 pathway (reduced p-ATR, p-CHK1, WEE1, CDC25A) and increased γH2AX foci. Co-IP confirmed KIF18B-ATR interaction, suggesting stabilization of DNA damage signaling. In vivo, KIF18B knockdown synergized with oxaliplatin, achieving > 80% tumor suppression and reduced Ki-67/p-ATR/p-CHK1 levels. In conclusion, KIF18B is a prognostic biomarker and therapeutic target in ESCC. Its inhibition overcomes oxaliplatin resistance by disrupting KIF18B-ATR interaction and ATR/CHK1-mediated DNA repair. Combining KIF18B targeting with chemotherapy or ATR inhibitors represents a promising strategy for refractory ESCC. - Source: PubMed
Publication date: 2026/05/27
Liu WeiWang QianruTan XiaoCao ChunyuTian Bole