CCNB1 Antibody (Center)
- Known as:
- CCNB1 Antibody (Center)
- Catalog number:
- AP11096c-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CCNB1 Antibody (Center)
Related genes to: CCNB1 Antibody (Center)
- Gene:
- CCNB1 NIH gene
- Name:
- cyclin B1
- Previous symbol:
- CCNB
- Synonyms:
- -
- Chromosome:
- 5q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-10
- Date modifiied:
- 2016-10-05
Related products to: CCNB1 Antibody (Center)
Related articles to: CCNB1 Antibody (Center)
- Cancer is characterized as a multifactorial disease due to their complex genetic and molecular mechanisms that often converge across tissue types. Shared oncogenic pathways can help us understand these functions and discover broad-spectrum therapeutics. Earlier, most studies focused on finding specific drivers for individual cancer types. However, researchers are now more interested in identifying common molecular patterns across different cancers and developing therapies that can target multiple pathways at once. This study aimed to understand the common oncogenic pathways between breast, ovarian and colorectal (BOC) cancers and identify possible multitargeted therapeutic drug molecules. To identify the common differentially expressed genes (DEGs), we analyzed three transcriptomic datasets and found a total of 128 DEGs. The protein-protein interaction (PPI) network study reveals the top-ranked, most significant hub targets, AURKA, CDK1 and CCNB1, as drug targets. Enrichment analysis with GO and KEGG pathways, as well as regulatory network (TFs and mRNAs) analysis, revealed common pathogenetic processes among BOC cancers. The AMG-900 exhibits the highest binding affinity scores of -10.8, -9.40, and -9.7 kcal/mol with the target proteins AURKA, CCNB1, and CDK1, respectively. The stability and structural flexibility of the selected protein-ligand complexes were validated by a large-scale (500 ns) molecular dynamics and MM-GBSA analyses, and the results indicate stable interactions for AURKA and CCNB1, while CDK1 showed comparatively reduced stability. The pharmacokinetic analysis revealed favorable drug-likeness and a manageable toxicity profile typical of anticancer agents. Therefore, the findings of this study propose that AMG-900 may serve as a promising multi-targeted candidate for further investigation in multi-target therapeutic strategies within precision oncology. Furthermore, these results require additional experimental (in vivo and in vitro) and clinical validation to confirm the potentiality and efficiency of this (AMG-900) lead compound. - Source: PubMed
Publication date: 2026/06/01
Sarker HriddhiFarid Farhad BinKamrun MargubaMasud EshaAhmed AsifMiah MamunRoy Neladre ShakerKumar NeerajAli Md Ahad - Pancreatic cancer mortality remains high due to late diagnosis and therapeutic resistance. The present study investigated acylglycerol kinase (AGK), which has been implicated in other tumors, in pancreatic cancer. Quantitative PCR, western blotting and immunohistochemistry analyses showed that AGK was markedly upregulated in pancreatic cancer tissues and cell lines and its expression associated with poor prognosis. Furthermore, functional studies using AGK knockdown and overexpression models demonstrated that AGK promoted cancer cell proliferation by upregulating proliferation‑associated genes, such as and . Mechanistically, AGK activates NF‑κB signaling pathway by facilitating p65 nuclear translocation and enhancing its phosphorylation. Additionally, CCK‑8 and colony formation assays further indicated that elevated AGK levels reduced sensitivity to therapeutic drugs and irradiation in pancreatic cancer cells. These findings revealed the critical role of AGK in pancreatic cancer progression and treatment resistance, identifying it as a potential novel therapeutic target and diagnostic marker. - Source: PubMed
Publication date: 2026/05/29
Han KunkunZhang QianyunGao ShengnanZhang JigangMei XiaoLi FeiXu XinLi ShuChen Guodong - Hepatocellular carcinoma (HCC) is one of the most common types of liver cancer, with a high mortality rate. Despite significant advances in HCC detection and treatment, problem remain persistence. Plant-derived natural products have always been a boon for novel medication development; in this case, is a traditional medicinal plant recognised for its therapeutic usefulness in a variety of diseases. However, its efficacy against HCC has never been tested. Therefore, this study was initiated using an integrated in-silico approach to determine whether -derived compounds could target hub genes associated in HCC. Extracted Differentially expressed genes from two GEO database and TCGA-LIHC using GEO2R tool and R software. Overlapped DEG, were then utilised to conduct cluster analysis and performed three centrality techniques which were then intersected to obtain hub genes. The compounds extracted from bark of using ethyl acetate and identified via mass spectrometry. These hub genes were then docked with the selected compounds obtained from the bark extract of and Simultaneous drug-likeness was assessed through ADMET followed by validation using MD simulation. Six hub genes BUB1, BUB1B, CCNA2, CCNB1, CDK1 and KIF11 were seen significantly upregulated in hepatocellular carcinoma. Out of 64 compounds only C2, C55, and C65 of displayed strong binding affinity as well as favourable drug-likeness. Molecular dynamics simulation validated the stability of these complexes' structures, but localised loop flexibility facilitated adaptation. At last, this pioneer study shown the potential of as promising leads to HCC open avenue for future research. - Source: PubMed
Publication date: 2026/05/26
Das TanusreeChoudhury ShuvasishChoudhury Manabendra Dutta - Chronic inorganic arsenic (iAs) exposure is a global public health concern and a well‑established risk factor for bladder cancer; however, the molecular mechanisms by which iAs exposure drives the transition from reversible injury to irreversible transformation remain poorly understood. Here, we investigated the role of the transcription factor forkhead box M1 (FOXM1) in this process by integrating public transcriptomic and clinical cohort analyses, protein-protein interaction and pathway enrichment analyses, chronic arsenic-exposed mouse models, arsenic speciation analysis, histopathological assessment, RNA sequencing, molecular validation, and functional assays in human urothelial cells. Bioinformatics analysis identified FOXM1 as a key node linking iAs-responsive genes to cell-cycle pathways, with its expression correlating with poor prognosis and tumor stemness in human bladder cancer cohorts. In a mouse model exposed to arsenic for 56, 120, and 365 days, we observed progressive bladder tissue injury accompanied by sustained FOXM1 upregulation. Transcriptomic profiling further established FOXM1 as a central network hub in arsenic-induced gene dysregulation. Using a chronic iAs-induced cellular reprogramming model in human urothelial cells, we demonstrated that chronic arsenic exposure drives FOXM1-dependent entry into an irreversible proliferative state after 3-4 months, which persists despite FOXM1 inhibition. Furthermore, FOXM1 overexpression synergized with iAs to enhance proliferative responses through downstream cell-cycle effectors CCNB1 and CDC25B. Collectively, these findings suggest that chronic iAs exposure promotes FOXM1-associated bladder epithelial alterations through cell cycle dysregulation, with FOXM1 representing a potential early intervention target in iAs-related bladder pathology. - Source: PubMed
Publication date: 2026/05/26
Kan HuiChen MenglanHu WanxuanYang NingZhang TongChen YuxuanYing XiaodongChen XushenRen Xuefeng - Kidney renal clear cell carcinoma (KIRC) is a highly aggressive and heterogeneous malignancy characterized by poor clinical outcomes and limited reliable prognostic biomarkers. This study performed a comprehensive bioinformatic analysis to evaluate the clinical and biological significance of threonine-tyrosine kinase (TTK/Mps1) in KIRC. Transcriptomic analyses demonstrated significant overexpression of TTK in tumor tissues, which was strongly associated with advanced stage, metastatic progression, and reduced patient survival. Multivariate regression confirmed TTK as an independent prognostic indicator with high diagnostic accuracy. Network and enrichment analyses revealed that TTK is embedded within a tightly connected mitotic regulatory module, primarily involving spindle assembly checkpoint signaling, G2/M transition control, and chromosome segregation processes. Key co-expressed genes included BUB1, CCNB1, CDK1, and CENPF, indicating a coordinated proliferative program. Pathway analysis further showed strong positive associations with oncogenic cell-cycle signatures and negative correlations with metabolic pathways. Immune profiling indicated that elevated TTK expression correlates with increased immune infiltration and is associated with alterations in the tumor microenvironment. Collectively, these findings suggest that TTK is associated with prognosis and may serve as a potential biomarker in KIRC, with its therapeutic relevance requiring further investigation. - Source: PubMed
Publication date: 2026/05/26
Singh AnuradhaLakkaniga Naga Rajiv