CCNB1 antibody
- Known as:
- CCNB1 (anti-)
- Catalog number:
- orb107007
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- CCNB1 antibody
Related genes to: CCNB1 antibody
- 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
Related articles to: CCNB1 antibody
- Bisphenol A (BPA), an environmental endocrine disruptor, is implicated in hepatocellular carcinoma (HCC), but its molecular mechanisms are unclear. This study employed an integrative computational framework to identify potential BPA-related molecular targets in HCC, assess their statistical clinical value, and generate hypotheses regarding their roles within the tumor microenvironment. BPA and HCC targets were retrieved from public databases and intersected with differentially expressed genes in HCC, identifying fifteen overlapping genes statistically enriched in cell cycle regulation, p53 signaling, and viral carcinogenesis. Six hub genes (MKI67, CCNA2, EZH2, CCNB1, CDK1, BIRC5) were significantly upregulated in HCC with high internal cross-validated diagnostic accuracy (AUC > 0.96), although these estimates may be susceptible to overfitting and require external validation. Molecular docking and dynamics simulations predicted stable BPA binding to six proteins (Ki67, Cyclin A2, EZH2, Cyclin B1, CDK1, Survivin), with van der Waals forces calculated as the primary driving energy contribution by MM-PBSA. The two-gene (CCNB1/EZH2) risk model showed statistical associations with patient survival, validated internally and externally, although its generalizability remains limited. Mendelian randomization provided genetic evidence consistent with a potential risk-associated role for CCNB1 and a protective-associated role for EZH2. Single-cell analysis localized high CCNB1 and EZH2 expression to malignant and proliferative T-cells, correlating with specific immune infiltration patterns and checkpoint expression. In conclusion, these computational findings suggest a statistical and structural association between BPA exposure and HCC-related core cell-cycle regulators (e.g., CCNB1/EZH2). The data generate the hypothesis that CCNB1 and EZH2 may serve as prognostic biomarkers and potential contributors to HCC biology, possibly through coordinated effects on cell cycle dysregulation and immune microenvironment remodeling, though direct evidence of in vivo molecular targeting by BPA or causal pathway activation is not established by this study. These findings provide novel insights into BPA's putative role in hepatocarcinogenesis and offer clues for future experimental validation regarding risk assessment and therapeutic strategies. - Source: PubMed
Publication date: 2026/05/12
Zeng FulingLai FuyanZeng Jiaxin - The grass carp reovirus (GCRV) infection poses a severe threat to grass carp because it triggers hemorrhagic disease using complex host-virus interactions but research on the early phases of GCRV infection is still lacking. To evaluate host responses to GCRV infection, in the current study we used Ctenopharyngodon idella kidney (CIK) cells as in vitro model infected with GCRV-I to conduct comparative experiments at different time points 0, 3, 6, 12, and 24h. GCRV infection caused cytopathic effects (CPEs) in (CIK) cells. Significant temporal variations in host gene expression were found by targeted qPCR studies and qPCR analysis demonstrated dynamic modulation of host gene expression. Significant variations between treated and control cells were shown by comparative expression profiling across different time points. High-throughput RNA sequencing (RNA-seq) revealed transcriptional reprogramming during infection, reflected by progressive elevation in differentially expressed genes, followed by qPCR validation. Notably, GO/KEGG enrichment analysis showed that GCRV-I activated the cholesterol, steroid, cell cycle, immune related and circadian regulation across all time points. Important genes with time-dependent expression patterns included dhcr7, cdk1 and irf3. Cell cycle regulators (ccnb1, cdc25b, wee1, cdc20) modulate cdk1 activity, separating transcriptional programs into irf3/tlr19 centered antiviral modules and dhcr7-centered cholesterol metabolism during early GCRV infection in CIK cells, according to our time-series RNA-seq and Weighted Gene Co-expression Network Analysis (WGCNA). These results provide possible targets for antiviral treatments in aquaculture and clarify complex host response to GCRV and provide a novel antiviral potential through cholesterol pathway. - Source: PubMed
Publication date: 2026/05/08
Younas WaqarZhang LeiShi MijuanYang HongCheng YingyinZhang WantingWang YapingXia Xiao-Qin - This study aimed to investigate the effects of resveratrol (RES) and carboplatin (CPT), alone and in combination, on cell viability, apoptosis, cell cycle progression, mitochondrial function, and oxidative stress in Y79 retinoblastoma (RB) cells. Particular emphasis was placed on evaluating the synergistic potential of the combination and elucidating the interconnected molecular mechanisms underlying its anticancer effects. Y79 cells were treated with RES, CPT, and their combinations. Cell viability and synergy were assessed using the MTT assay and combination index (CI) analysis. Apoptosis (annexin V/PI), cell cycle distribution (propidium iodide (PI) staining), intracellular ROS production (DCFH-DA), and mitochondrial membrane potential (JC-1) were evaluated by flow cytometry. ROS dependency was further examined using N-acetylcysteine (NAC) pretreatment. Expression levels of apoptosis- and cell cycle-related genes (, , , , , and ) were analyzed by RT-qPCR. Cytoskeletal alterations were assessed by immunocytochemistry. In addition, the antitumor effects of the combination were validated in a three-dimensional (3D) tumor spheroid model. RES and CPT reduced cell viability in a dose- and time-dependent manner and demonstrated synergistic effects (CI < 1) at selected concentrations. Combination treatment significantly increased apoptosis, induced G2/M phase arrest, enhanced ROS accumulation, and promoted mitochondrial depolarization compared with single-agent treatments. NAC pretreatment attenuated ROS generation and partially restored cell viability, supporting a contributory role of oxidative stress in combination-induced cytotoxicity. At the transcriptional level, the RES + CPT combination significantly increased the / ratio and upregulated and expression, while downregulating and , consistent with mitochondrial apoptotic activation and G2/M arrest. Immunocytochemical analysis revealed pronounced cytoskeletal disruption and apoptotic morphology in the combination group. Importantly, in the 3D spheroid model, co-treatment markedly reduced spheroid size and viability and enhanced cell death compared with monotherapies. The combination of RES and CPT exerts a synergistic anticancer effect in Y79 RB cells through coordinated mechanisms involving ROS accumulation, mitochondrial dysfunction, caspase activation, and G2/M phase arrest. The attenuation of cytotoxicity by NAC and the validation of efficacy in a 3D tumor spheroid model strengthen the mechanistic relevance of these findings. These results support further preclinical investigation of this combination strategy in in vivo models and normal retinal cell systems. - Source: PubMed
Publication date: 2026/04/13
Maçin AydınDuman ErkanÖzdemir İlhanTuncer Mehmet Cudi - Brain metastasis (BM) represents a significant clinical challenge in advanced breast cancer, yet the molecular mechanisms driving breast cancer brain metastasis (BCBM) remain incompletely characterized. This study aims to identify key molecular pathways and hub genes specifically associated with BCBM through comprehensive bioinformatic analyses. Gene Set Enrichment Analysis (GSEA), differential gene expression analysis, and weighted gene co-expression network analysis (WGCNA) were performed using two independent GEO datasets (GSE191230 and GSE43837). Protein-protein interaction (PPI) networks were constructed to visualize functional interconnections among dysregulated genes. Survival analyses were conducted using the Kaplan-Meier Plotter database to evaluate the prognostic significance of identified hub genes. GSEA revealed significant upregulation of metabolic pathways (mTORC1 signaling, glycolysis, oxidative phosphorylation) and downregulation of immune-related pathways in BCBM compared to primary tumors. Integrative analysis identified 34 consistently dysregulated genes across datasets, from which 12 hub genes were validated. Among these, RRM2, CDCA8, CCNB1, LMNB2, FANCI, NCAPH, YWHAZ, and ESPL1 demonstrated brain-specific over-expression compared to other metastatic sites. Functional enrichment analysis highlighted cell cycle dysregulation as a critical mechanism in BCBM, and all hub genes showed significant association with poor prognosis in breast cancer patients. This study identifies a unique molecular profile of BCBM characterized by cell cycle dysregulation, metabolic reprogramming, and immune microenvironment alterations. The brain-specific expression patterns of these hub genes represent potential biomarkers for BCBM risk assessment and novel therapeutic targets, providing a basis for precision medicine development. - Source: PubMed
Publication date: 2026/04/13
Ting Wei-YiLu Yueh-HsunLin Che-Ming - Lactate, an energy source and metabolic by-product, has been implicated in cancer progression, but its role in colorectal cancer (CRC) remains incompletely understood. This study investigated the clinical significance, biological effects, and transcriptomic responses of CRC cells to lactate. In human CRC specimens, lactate levels were positively associated with advanced clinical stage and poorer disease-free survival. Functional assays showed that lactate promoted malignant cellular behaviors in both SW480 and HCT116 cells, while pH-control experiments suggested that these effects were not merely due to extracellular acidification alone. RNA sequencing in SW480 cells identified 1,418 differentially expressed genes after lactate treatment. GO and KEGG analyses revealed alterations in multiple metabolic and signaling pathways. qRT-PCR validated the alterations of representative genes, including HK2, VEGFA, JUNB, CCNB1, MAPK4, and COX2. In addition, flow cytometry showed activation of NF-κB and HIF-1α signaling following lactate treatment, and pharmacological inhibition of either pathway significantly attenuated the lactate-induced malignant phenotypes. Together, these findings provide transcriptomic and functional evidence that lactate promotes malignant phenotypes in CRC cells and offer exploratory mechanistic insights into the involvement of NF-κB and HIF-1α signaling. - Source: PubMed
Publication date: 2026/05/02
Li ShujuanFeng ShiweiLi XuannaSu RanDeng JinhuaCheng SijingHou Yujie