Cyclin-B1-mediated inhibition of excess separase is required for timely chromosome disjunction

Antisense oligonucleotides (ASO) represent an attractive trend as specific targeting molecules but sustain poor cellular uptake meanwhile superparamagnetic iron oxide nanoparticles (SPIONs) offer stability of ASO and improved cellular uptake. In the present work we aimed to functionalize SPIONs with ASO targeting the mRNA of Cyclin B1 which represents a potential cancer target and to explore its anticancer activity. For that purpose, four different SPIONs-ASO conjugates, S-M (1–4), were designated depending on the sequence of ASO and constructed by crosslinking carboxylated SPIONs to amino labeled ASO. The impact of S-M (1–4) on the level of Cyclin B1, cell cycle, ROS and viability of the cells were assessed by flowcytometry. The results showed that S-M3 and S-M4 reduced the level of Cyclin B1 by 35 and 36%, respectively. As a consequence to downregulation of Cyclin B1, MCF7 cells were shown to be arrested at G2/M phase (60.7%). S-M (1–4) led to the induction of ROS formation in comparison to the untreated control cells. Furthermore, S-M (1–4) resulted in an increase in dead cells compared to the untreated cells and SPIONs-treated cells. In conclusion, targeting Cyclin B1 with ASO-coated SPIONs may represent a specific biocompatible anticancer strategy.

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Expression of histone H3, p53, cyclin D1, and cyclin B1 in oral mucosal lesions

Oral Medicine & Pathology ◽

10.3353/omp.13.119 ◽

2009 ◽

Vol 13 (4) ◽

pp. 119-126

Author(s):

Yoshimitsu Bamba ◽

Tetsunari Nishikawa ◽

Akio Tanaka

Keyword(s):

Cyclin D1 ◽

Histone H3 ◽

Cyclin B1 ◽

Oral Mucosal Lesions ◽

Mucosal Lesions

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Activation of bovine oocytes by protein synthesis inhibitors: new findings on the role of MPF/MAPKs†

Biology of Reproduction ◽

10.1093/biolre/ioab019 ◽

2021 ◽

Author(s):

Cecilia Valencia ◽

Felipe Alonso Pérez ◽

Carola Matus ◽

Ricardo Felmer ◽

María Elena Arias

Keyword(s):

Protein Synthesis ◽

Kinase Activity ◽

Cyclin B1 ◽

Protein Synthesis Inhibitors ◽

Vitro Fertilization ◽

New Findings ◽

Bovine Oocytes ◽

Dependent Pathway

Abstract The present study evaluated the mechanism by which protein synthesis inhibitors activate bovine oocytes. The aim was to analyze the dynamics of MPF and MAPKs. MII oocytes were activated with ionomycin (Io), ionomycin+anisomycin (ANY) and ionomycin+cycloheximide (CHX) and by in vitro fertilization (IVF). The expression of cyclin B1, p-CDK1, p-ERK1/2, p-JNK, and p-P38 were evaluated by immunodetection and the kinase activity of ERK1/2 was measured by enzyme assay. Evaluations at 1, 4, and 15 hours postactivation (hpa) showed that the expression of cyclin B1 was not modified by the treatments. ANY inactivated MPF by p-CDK1Thr14-Tyr15 at 4 hpa (P < 0.05), CHX increased pre-MPF (p-CDK1Thr161 and p-CDK1Thr14-Tyr15) at 1 hpa and IVF increased p-CDK1Thr14-Tyr15 at 17 hours postfertilization (hpf) (P < 0.05). ANY and CHX reduced the levels of p-ERK1/2 at 4 hpa (P < 0.05) and its activity at 4 and 1 hpa, respectively (P < 0.05). Meanwhile, IVF increased p-ERK1/2 at 6 hpf (P < 0.05); however, its kinase activity decreased at 6 hpf (P < 0.05). p-JNK in ANY, CHX, and IVF oocytes decreased at 4 hpa (P < 0.05). p-P38 was only observed at 1 hpa, with no differences between treatments. In conclusion, activation of bovine oocytes by ANY, CHX, and IVF inactivates MPF by CDK1-dependent specific phosphorylation without cyclin B1 degradation. ANY or CHX promoted this inactivation, which seemed to be more delayed in the physiological activation (IVF). Both inhibitors modulated MPF activity via an ERK1/2-independent pathway, whereas IVF activated the bovine oocytes via an ERK1/2-dependent pathway. Finally, ANY does not activate the JNK and P38 kinase pathways.

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Cyclin B1 transcription is enhanced by the p300 coactivator and regulated during the cell cycle by a CHR-dependent repression mechanism

FEBS Letters ◽

10.1016/s0014-5793(03)00028-0 ◽

2003 ◽

Vol 536 (1-3) ◽

pp. 66-70 ◽

Cited By ~ 43

Author(s):

Mark Wasner ◽

Katrin Tschöp ◽

Katja Spiesbach ◽

Ulrike Haugwitz ◽

Cindy Johne ◽

...

Keyword(s):

Cell Cycle ◽

Cyclin B1

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Cyclin B1 acts as a tumor microenvironment-related cancer promoter and prognostic biomarker in hepatocellular carcinoma

Journal of International Medical Research ◽

10.1177/03000605211016265 ◽

2021 ◽

Vol 49 (5) ◽

pp. 030006052110162

Author(s):

Yangming Hou ◽

Xin Wang ◽

Junwei Wang ◽

Xuemei Sun ◽

Xinbo Liu ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Tumor Microenvironment ◽

Proportional Hazards ◽

Enrichment Analysis ◽

Gene Signature ◽

Cyclin B1 ◽

Cox Proportional Hazards ◽

Gene Set Enrichment Analysis ◽

Tumor Promoter ◽

Protein Protein Interaction

Objectives The present study aimed to develop a gene signature based on the ESTIMATE algorithm in hepatocellular carcinoma (HCC) and explore possible cancer promoters. Methods The ESTIMATE and CIBERSORT algorithms were applied to calculate the immune/stromal scores and the proportion of tumor-infiltrating immune cells (TICs) in a cohort of HCC patients. The differentially expressed genes (DEGs) were screened by Cox proportional hazards regression analysis and protein–protein interaction (PPI) network construction. Cyclin B1 (CCNB1) function was verified using experiments. Results The stromal and immune scores were associated with clinicopathological factors and recurrence-free survival (RFS) in HCC patients. In total, 546 DEGs were up-regulated in low score groups, 127 of which were associated with RFS. CCNB1 was regarded as the most predictive factor closely related to prognosis of HCC and could be a cancer promoter. Gene Set Enrichment Analysis (GSEA) and CIBERSORT analyses indicated that CCNB1 levels influenced HCC tumor microenvironment (TME) immune activity. Conclusions The ESTIMATE signature can be used as a prognosis tool in HCC. CCNB1 is a tumor promoter and contributes to TME status conversion.

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