Cyclin B1 expression as an independent prognostic factor for lung adenocarcinoma and its potential pathways
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PROVIDER: PRJNA855641 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the functional mechanism of CCNB1 in lung adenocarcinoma, we knocked down CCNB1 in H1299 cell line and performed sequencing analysis.We then performed gene expression profiling analysis using data obtained from RNA-seq.
2022-07-08 | GSE207450 | GEO
Project description:After severe renal injury, renal tubular epithelial cells (TECs) will be arrested in G2/M phase, and the arrested cells will be aging, showing senescence related secretory phenotype (SASP), which mediates renal fibrosis by secreting fibrogenic cytokines. Cyclin B1 is an important protein that promotes G2/M phase transition of cell cycle. Its role in renal fibrosis mediated by G2/M arrest of TECs is unknown. The aim of this study was to investigate the role of cyclin B1 in renal fibrosis induced by TECs G2/M arrest and its mechanism
2024-01-01 | GSE224039 | GEO
Project description:Mitosis in early embryos often proceeds at a rapid pace, but how this pace is achieved is not understood. Here we show that cyclin B3 is the dominant driver of rapid embryonic mitoses in the C. elegans embryo. Cyclins B1 and B2 support slow mitosis (NEBD to Anaphase ~600s) but the presence of cyclin B3 dominantly drives the ~3-fold faster mitosis observed in wildtype. Multiple mitotic events are slowed down in Cyclin B1&B2-driven mitosis and cyclin B3-associated Cdk1 H1 kinase activity is ~25-fold more active than cyclin B1-associated Cdk1. Addition of cyclin B1 to fast cyclin B3-only mitosis introduces an ~60s delay between completion of chromosome alignment and anaphase onset; this delay, which is important for segregation fidelity, is dependent on inhibitory phosphorylation of the anaphase activator Cdc20. Thus, cyclin B3 dominance, coupled to a cyclin B1-dependent delay that acts via Cdc20 phosphorylation, sets the rapid pace and ensures mitotic fidelity in the early C. elegans embryo.
2024-07-29 | PXD053811 | Pride
Project description:BackgroundGlucosamine-Phosphate N-Acetyltransferase 1 (GNPNAT1) is a critical enzyme in the biosynthesis of uridine diphosphate-N-acetylglucosamine. It has many important functions, such as protein binding, monosaccharide binding, and embryonic development and growth. However, the role of GNPNAT1 in lung adenocarcinoma (LUAD) remains unclear.MethodsIn this study, we explored the expression pattern and prognostic value of GNPNAT1 in LUAD across TCGA and GEO databases and assessed its independent prognostic value via Cox analysis. LinkedOmics and GEPIA2 were applied to investigate coexpression and functional networks associated with GNPNAT1. The TIMER web tool was deployed to assess the correlation between GNPNAT1 and the main six types of tumor-infiltrating immune cells. Besides, the correlations between GNPNAT1 and the LUAD common genetic mutations, TMB, and immune signatures were examined.ResultsGNPNAT1 was validated upregulated in tumor tissues in TCGA-LUAD and GEO cohorts. Moreover, in both TCGA and GEO cohorts, high GNPNAT1 expression was found to be associated with poor overall survival. Cox analysis showed that high GNPNAT1 expression was an independent risk factor for LUAD. Functional network analysis suggested that GNPNAT1 regulates cell cycle, ribosome, proteasome, RNA transport, and spliceosome signaling through pathways involving multiple cancer-related kinases and E2F family. In addition, GNPNAT1 correlated with infiltrating levels of B cells, CD4+ T cells, and dendritic cells. B cells and dendritic cells could predict the outcome of LUAD, and B cells and CD4+ T cells were significant independent risk factors. The TMB and mutations of KRAS, EGFR, STK11, and TP53 were correlated with GNPNAT1. At last, the correlation analysis showed GNPNAT1 correlated with most of the immune signatures we performed.ConclusionOur findings showed that GNPNAT1 was correlated to the prognosis and immune infiltration of LUAD. In particular, the tight relationship between GNPNAT1 and B cell marker genes may be the epicenter of the immune response and one of the key factors affecting the prognosis. Our findings laid the foundation for further research on the immunomodulatory role of GNPNAT1 in LUAD.
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Project description:How the cell rapidly and completely reorganises its architecture when it divides is a problem that has fascinated for almost 150 years. We now know that the core regulatory machinery is highly conserved in eukaryotes but how these multiple protein kinases, protein phosphatases, and ubiquitin ligases are coordinated in space and time to remodel the cell in a matter of minutes remains a major question. Cyclin B-Cdk is the primary kinase that drives mitotic remodelling and here we show that it is targeted to the nuclear pore complex (NPC) by binding an acidic face of the kinetochore checkpoint protein, MAD1, where it coordinates NPC disassembly with kinetochore assembly. This localised Cyclin B1-Cdk1 activity is needed for the proper release of MAD1 from the embrace of TPR at the nuclear pore so that it can be recruited to kinetochores before nuclear envelope breakdown to maintain genomic stability.
2020-06-29 | PXD017202 | Pride
Project description:When cells enter mitosis, the anaphase-promoting complex/cyclosome (APC/C) is activated by phosphorylation and binding of Cdc20. The RXXL destruction box (D-box) of cyclin B1 only binds Cdc20 after release of the spindle checkpoint in metaphase, initiating cyclin B1 ubiquitination upon chromosome bi-orientation. However, we found that cyclin B1, through Cdk1 and Cks, is targeted to the phosphorylated APC/C(Cdc20) at the start of prometaphase, when the spindle checkpoint is still active. Here, we show that MASTL is essential for cyclin B1 recruitment to the mitotic APC/C and that this occurs entirely independently of Cdc20. Importantly, MASTL-directed binding of cyclin B1 to spindle checkpoint-inhibited APC/C(Cdc20) critically supports efficient cyclin B1 destruction after checkpoint release. A high incidence of anaphase bridges observed in response to MASTL RNAi may result from cyclin B1 remaining after securin destruction, which is insufficient to keep MASTL-depleted cells in mitosis but delays the activation of separase.
| S-EPMC4400591 | biostudies-literature
Project description:Pisolithus sp. B1 Transcriptome - B1
| PRJNA572143 | ENA
Project description:In eukaryotes, cyclin/CDK complexes drive cells through DNA replication and mitosis, establising cell cycle temporal order. The fission yeast S. pombe is able to function with a single cyclin/CDK complex, with cell cycle order emerging from differential substrate sensitivities to CDK activity. What influence cyclin specificity has upon the cell cycle in this situation is currently unknown. Here we show that in a system that is reliant on a single cyclin for both the G1/S and G2/M transition, cyclin specificity is not needed for the G1/S transition, but instead is required for the G2/M transition and correct localisation of cyclin/CDK to the yeast centrosome equivalent, the SPB. This loss of centrosome localisation was also seen in human cells expressing mutant Cyclin B1, suggesting conservation of function. In fission yeast, although interphase centrosomal localisation is lost, mitotic SPB localisation remains. This hitherto unknown second localisation method is dependent on Polo kinase, suggesting a finer spatiotemporal control of cyclin/CDK during cell cycle progression than previously known. Thus, cyclin specificity is intrinsically twinned with spatial control of cyclin/CDK, and we suggest that this regulation may be conserved through evolution.
2019-05-27 | PXD011987 | Pride
Project description:Microtubule inhibitors are widely used in cancer chemotherapy. These drugs characteristically induce mitotic arrest and cell death but the mechanisms linking the two are not firmly established. One of the problems is that cancer cells vary widely in their sensitivity to these agents, and thus comparison of data from different systems is difficult. To alleviate this problem we sought to molecularly induce mitotic death and study its mechanisms, by expressing non-degradable cyclin B (R42A) in HeLa cells. However, this approach failed to induce significant mitotic arrest, Cdk1 activation, or phosphorylation of anti-apoptotic Bcl-2 proteins, all characteristics of cells treated with microtubule inhibitors. Furthermore, cyclin B1-R42A induced rapid cell death, and when expressed in synchronized cells, cell death occurred in G1 phase. Decreasing the plasmid concentration reduced transfection efficiency but restored mitotic arrest and eliminated non-specific death. These results show that inappropriate overexpression of cyclin B1 causes non-specific cell death and suggest caution in its use for the study of mitotic events.
| S-EPMC4240608 | biostudies-literature
Project description:Novosphingobium sp. B1 strain:B1 Genome sequencing
| PRJNA368292 | ENA