Ask about this productRelated 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
- 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 - -Aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the central nervous system and is involved in the development of neural tissue as well as the regulation of its functions. Meanwhile, GABA has also been demonstrated to confer multiple physiological benefits, including alleviating stress and improving metabolic homeostasis. This study investigated GABA effects on proliferation, differentiation, and temperature stress protection of bovine skeletal muscle satellite cells (BSCs). - Source: PubMed
Publication date: 2026/04/14
Manzoor AbidNaseem SajidaFu ZhiqiRuan ChaohuiLiu XuYan ChunriChoi SeonghoLi Xiangzi - Malachite green (MG), a synthetic dye, has turned into a major risk to human health, because of its toxicity of teratogenic, genotoxic, carcinogenic, and immunosuppressive properties. And the result of ADMETLAB 2.0 platform prediction shows that MG is highly toxic to the respiratory system in our study. However, no study has conducted to verify and explain the association between MG and lung adenocarcinoma (LUAD). In the current investigation, a total of 34 candidate target genes that might be involved in MG-mediated modulation in LUAD were identified and screened through integrated machine learning algorithms, including LASSO regression and random forest analysis. Subsequent functional annotation revealed that these genes were predominantly enriched in biological processes associated with the cell cycle. Meanwhile, pathway analysis indicated that the majority of these genes were closely linked to the p53 signaling pathway. Furthermore, molecular docking simulation validated that MG could stably and specifically bind to TP53, CCNB1, and MAPK1 proteins. In summary, our results demonstrated that MG may participate in the tumorigenesis and progression of LUAD, mainly by regulating the cell cycle via the p53 and MAPK signaling pathways. Among these, TP53, CCNB1, and MAPK1 could act as crucial candidate targets in MG‑mediated LUAD development. These findings provide novel insights into the molecular mechanisms underlying the role of MG in LUAD, and lay a theoretical basis for the future prevention and targeted therapy of LUAD. - Source: PubMed
Qu ShaoboYang ZhichaoZhang ShuaiHou Yongwang