Characterization of cyclin B1 expression in human cancer cell lines by a new three-parameter BrdUrd/Cyclin B1/DNA analysis

Faretta, Mario; Bergamaschi, Daniele; Taverna, Stefano; Ronzoni, Simona; Pantarotto, M.; Mascellani, E; Cappella, Paolo; Ubezio, Paolo; Erba, Eugenio

doi:10.1002/(sici)1097-0320(19980101)31:1<53::aid-cyto7>3.0.co;2-k

Cited by 14 publications

(7 citation statements)

References 22 publications

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“…We further demonstrate that 6-OAP induces mitotic arrest by observing α-tubulin staining and pH3 (S10) expression [33] in these cells upon 6-OAP treatment (Figure 2, D through F). Previous studies reported that cyclin B1 accumulates in S-phase, reaches a maximum at mitosis, and is then rapidly degraded at the metaphase/anaphase transition [54], [55]. We demonstrate that 6-OAP treatment leads to inappropriate accumulation of cyclin B1 (Figure 3, A and B).…”

Section: Discussionsupporting

confidence: 61%

Small Compound 6-O-Angeloylplenolin Induces Mitotic Arrest and Exhibits Therapeutic Potentials in Multiple Myeloma

Liu

Chen²,

Liang

et al. 2011

PLoS ONE

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BackgroundMultiple myeloma (MM) is a disease of cell cycle dysregulation while cell cycle modulation can be a target for MM therapy. In this study we investigated the effects and mechanisms of action of a sesquiterpene lactone 6-O-angeloylplenolin (6-OAP) on MM cells.Methodology/Principal FindingsMM cells were exposed to 6-OAP and cell cycle distribution were analyzed. The role for cyclin B1 to play in 6-OAP-caused mitotic arrest was tested by specific siRNA analyses in U266 cells. MM.1S cells co-incubated with interleukin-6 (IL-6), insulin-like growth factor-I (IGF-I), or bone marrow stromal cells (BMSCs) were treated with 6-OAP. The effects of 6-OAP plus other drugs on MM.1S cells were evaluated. The in vivo therapeutic efficacy and pharmacokinetic features of 6-OAP were tested in nude mice bearing U266 cells and Sprague-Dawley rats, respectively. We found that 6-OAP suppressed the proliferation of dexamethasone-sensitive and dexamethasone-resistant cell lines and primary CD138+ MM cells. 6-OAP caused mitotic arrest, accompanied by activation of spindle assembly checkpoint and blockage of ubiquitiniation and subsequent proteasomal degradation of cyclin B1. Combined use of 6-OAP and bortezomib induced potentiated cytotoxicity with inactivation of ERK1/2 and activation of JNK1/2 and Casp-8/-3. 6-OAP overcame the protective effects of IL-6 and IGF-I on MM cells through inhibition of Jak2/Stat3 and Akt, respectively. 6-OAP inhibited BMSCs-facilitated MM cell expansion and TNF-α-induced NF-κB signal. Moreover, 6-OAP exhibited potent anti-MM activity in nude mice and favorable pharmacokinetics in rats.Conclusions/SignificanceThese results indicate that 6-OAP is a new cell cycle inhibitor which shows therapeutic potentials for MM.

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Section: Discussionsupporting

confidence: 61%

Small Compound 6-O-Angeloylplenolin Induces Mitotic Arrest and Exhibits Therapeutic Potentials in Multiple Myeloma

Liu

Chen²,

Liang

et al. 2011

PLoS ONE

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“…The interpretation that PAF-treated retinal progenitor cells arrest at the S/G2 transition was further strengthened by the combination of the blockade of IKNM at the basal side of the proliferating cells with the abrogation of cyclin B1 build-up, which would be expected to occur along the S/G2 transition and during G2 [58], [59]. Indeed, IKNM facilitates the assignment of events to the S/G2 transition and early G2, as opposed to late G2 and the G2/M transition [55], [60], [61].…”

Section: Discussionmentioning

confidence: 99%

Platelet Activating Factor Blocks Interkinetic Nuclear Migration in Retinal Progenitors through an Arrest of the Cell Cycle at the S/G2 Transition

et al. 2011

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Nuclear migration is regulated by the LIS1 protein, which is the regulatory subunit of platelet activating factor (PAF) acetyl-hydrolase, an enzyme complex that inactivates the lipid mediator PAF. Among other functions, PAF modulates cell proliferation, but its effects upon mechanisms of the cell cycle are unknown. Here we show that PAF inhibited interkinetic nuclear migration (IKNM) in retinal proliferating progenitors. The lipid did not, however, affect the velocity of nuclear migration in cells that escaped IKNM blockade. The effect depended on the PAF receptor, Erk and p38 pathways and Chk1. PAF induced no cell death, nor a reduction in nucleotide incorporation, which rules out an intra-S checkpoint. Notwithstanding, the expected increase in cyclin B1 content during G2-phase was prevented in the proliferating cells. We conclude that PAF blocks interkinetic nuclear migration in retinal progenitor cells through an unusual arrest of the cell cycle at the transition from S to G2 phases. These data suggest the operation, in the developing retina, of a checkpoint that monitors the transition from S to G2 phases of the cell cycle.

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“…The denaturation of DNA can be varied with time, only partially allowing the use of DNA probes staining such as propidium iodide (PI) , 7-aminoactynomycin D, TOPRO-3, which interacts DNA requiring double helix conformation. The use of acid denaturation may not be the most appropriate method if it is necessary to maintain cellular (scatters) morphology, surface antigenicity or cell constituents such as cyclins (Faretta et al, 1998) or phosphorylation of signaling proteins (Gasparri et al, 2006) during multiparameter analysis. 3.…”

Section: Mps-1 Kinase Inhibitor (Nms-p715)mentioning

confidence: 99%

Assessment of Cell Cycle Inhibitors by Flow Cytometry

Cappella¹,

Moll²

2011

Drug Discovery and Development - Present and Future

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Characterization of cyclin B1 expression in human cancer cell lines by a new three-parameter BrdUrd/Cyclin B1/DNA analysis

Cited by 14 publications

References 22 publications

Small Compound 6-O-Angeloylplenolin Induces Mitotic Arrest and Exhibits Therapeutic Potentials in Multiple Myeloma

Small Compound 6-O-Angeloylplenolin Induces Mitotic Arrest and Exhibits Therapeutic Potentials in Multiple Myeloma

Platelet Activating Factor Blocks Interkinetic Nuclear Migration in Retinal Progenitors through an Arrest of the Cell Cycle at the S/G2 Transition

Assessment of Cell Cycle Inhibitors by Flow Cytometry

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