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Cyclin B1 expression as an independent prognostic factor for lung adenocarcinoma and its potential pathways

ABSTRACT: Cyclin B1 expression as an independent prognostic factor for lung adenocarcinoma and its potential pathways

PROVIDER: PRJNA855641 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19976756_1.fastq.gz	Fastqsanger.gz
	SRR19976756_2.fastq.gz	Fastqsanger.gz
	SRR19976757_1.fastq.gz	Fastqsanger.gz
	SRR19976757_2.fastq.gz	Fastqsanger.gz
	SRR19976758_1.fastq.gz	Fastqsanger.gz

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Cyclin B1 expression as an independent prognostic factor for lung adenocarcinoma and its potential pathways

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.

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Ligand-independent integrin beta1 signaling supports lung adenocarcinoma development

Project description:Integrins, the principal extracellular matrix (ECM) receptors of the cell, promote cell adhesion, migration, and proliferation, which are key events for cancer growth and metastasis. To date, most integrin-targeted cancer therapeutics have disrupted integrin-ECM interactions, which are viewed as critical for integrin functions. However, such agents have failed to improve cancer patient outcomes. We show that integrin b1, a highly expressed subunit in lung epithelium, is required for lung adenocarcinoma development in a carcinogen-induced mouse model. Likewise, human lung adenocarcinoma cell lines with integrin b1 deletion failed to form colonies in soft agar and tumors in mice. Mechanistically, we demonstrate that these effects do not require integrin b1-mediated adhesion to ECM but are dependent on integrin b1 cytoplasmic tail-mediated activation of focal adhesion kinase (FAK). Together, these studies support a critical role for integrin b1 in lung tumorigenesis that is mediated through constitutive, ECM-binding independent signaling involving the cytoplasmic tail.

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Cyclin B1 expression as an independent prognostic factor for lung adenocarcinoma and its potential pathways.

Project description:Although great progress has been made in the early diagnosis and targeted therapy of lung adenocarcinoma (LUAD), the survival of patients with LUAD remains unsatisfactory. There is an urgent requirement for new biomarkers to guide the diagnosis, prognosis and treatment of LUAD. Following an initial bioinformatics screen, the present study focused on cyclin B1 (CCNB1) in LUAD. A total of 94 patients with LUAD from a single hospital were included in the study. CCNB1 protein expression was detected and scored in 94 LUAD samples and 30 normal tissue samples by immunohistochemistry. The associations between CCNB1 expression and the clinicopathological features of the patients with LUAD were analyzed. Furthermore, the relationship between prognosis and the CCNB1 expression level was analyzed using Cox regression and survival analyses. Weighted gene co-expression network analysis and RNA-sequencing were also applied to identify the potential molecular mechanisms of CCNB1 in LUAD. CCNB1 was highly expressed in patients with LUAD and was associated with poor prognosis. It may affect the expression of CPLX1, PPIF, SRPK2, KRT8, SLC20A1 and CBX2 genes and function via different pathways. CCNB1 has the potential to become a novel prognostic target for LUAD.

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Cyclin B1 deficiency in renal tubular epithelial cells promotes kidney ageing and fibrosis in mice

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

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Cyclin B3 is a dominant fast-acting cyclin that drives rapid early embryonic mitoses

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.

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Project description:To evaluate the prognostic relevance of molecular subtypes and key transcription factors in pancreatic ductal adenocarcinoma (PDAC), we performed gene expression analysis of whole-tumor tissue obtained from 118 surgically resected PDAC and 13 control samples.

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MASTL promotes cyclin B1 destruction by enforcing Cdc20-independent binding of cyclin B1 to the APC/C.

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Cyclin B1-Cdk1 binds MAD1 and facilitates its release from the nuclear pore complex to ensure a robust Spindle Assembly Checkpoint

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.

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Ligand-independent integrin beta1 signaling supports lung adenocarcinoma development

Project description:Ligand-independent integrin beta1 signaling supports lung adenocarcinoma development

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