Vanadocene dichloride inhibits cell proliferation by targeting Aurora B

Metallomics ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1099-1106 ◽  
Author(s):  
Tzu-Chia Ting ◽  
Meng-Ya Chang ◽  
Tzu-Yen Hsu ◽  
Wen-Pin Wang ◽  
Yi-Jen Hsieh ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Aurora B ◽  
Vanadocene Dichloride

Vanadocene dichloride induces chromosome misalignment by inhibiting Aurora B activity.

Aurora-B expression and its correlation with cell proliferation and metastasis in oral cancer

2007 ◽  
Vol 450 (3) ◽  
pp. 297-302 ◽  
Author(s):  
Guangying Qi ◽  
Ikuko Ogawa ◽  
Yasusei Kudo ◽  
Mutsumi Miyauchi ◽  
B. S. M. S. Siriwardena ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Oral Cancer ◽  
Aurora B ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

Aurora B expression directly correlates with prostate cancer malignancy and influence prostate cell proliferation

The Prostate ◽  
2006 ◽  
Vol 66 (3) ◽  
pp. 326-333 ◽  
Author(s):  
Paolo Chieffi ◽  
Laura Cozzolino ◽  
Annamaria Kisslinger ◽  
Silvana Libertini ◽  
Stefania Staibano ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Aurora B ◽  
Prostate Cell

scholarly journals Combination Treatment of OSI-906 with Aurora B Inhibitor Reduces Cell Viability via Cyclin B1 Degradation-Induced Mitotic Slippage

2021 ◽  
Vol 22 (11) ◽  
pp. 5706
Author(s):  
Yuki Ikeda ◽  
Ryuji Yasutake ◽  
Ryuzaburo Yuki ◽  
Youhei Saito ◽  
Yuji Nakayama
Keyword(s):  
Cell Proliferation ◽  
Cell Viability ◽  
Combination Treatment ◽  
Spindle Assembly Checkpoint ◽  
Time Lapse ◽  
Cyclin B1 ◽  
Suppressive Effect ◽  
Aurora B ◽  
Mitotic Slippage ◽  
Chromosome Alignment

Insulin-like growth factor 1 receptor (IGF1R), a receptor-type tyrosine kinase, transduces signals related to cell proliferation, survival, and differentiation. We recently reported that OSI-906, an IGF1R inhibitor, in combination with the Aurora B inhibitor ZM447439 suppresses cell proliferation. However, the mechanism underlying this suppressive effect is yet to be elucidated. In this study, we examined the effects of combination treatment with OSI-906 and ZM447439 on cell division, so as to understand how cell proliferation was suppressed. Morphological analysis showed that the combination treatment generated enlarged cells with aberrant nuclei, whereas neither OSI-906 nor ZM447439 treatment alone caused this morphological change. Flow cytometry analysis indicated that over-replicated cells were generated by the combination treatment, but not by the lone treatment with either inhibitors. Time-lapse imaging showed mitotic slippage following a severe delay in chromosome alignment and cytokinesis failure with furrow regression. Furthermore, in S-trityl-l-cysteine–treated cells, cyclin B1 was precociously degraded. These results suggest that the combination treatment caused severe defect in the chromosome alignment and spindle assembly checkpoint, which resulted in the generation of over-replicated cells. The generation of over-replicated cells with massive aneuploidy may be the cause of reduction of cell viability and cell death. This study provides new possibilities of cancer chemotherapy.

scholarly journals Targeting Insulin-Like Growth Factor 1 Receptor Delays M-Phase Progression and Synergizes with Aurora B Inhibition to Suppress Cell Proliferation

2020 ◽  
Vol 21 (3) ◽  
pp. 1058
Author(s):  
Akane Yamagishi ◽  
Yuki Ikeda ◽  
Masayoshi Ikeuchi ◽  
Ryuzaburo Yuki ◽  
Youhei Saito ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Cancer Progression ◽  
Spindle Assembly Checkpoint ◽  
Aurora B ◽  
Insulin Like Growth Factor ◽  
Altered Expression ◽  
M Phase ◽  
Igf1r Inhibitor ◽  
The Impact

The insulin-like growth factor 1 receptor (IGF1R) is a receptor-type tyrosine kinase that transduces signals related to cell proliferation, differentiation, and survival. IGF1R expression is often misregulated in tumor cells, but the relevance of this for cancer progression remains unclear. Here, we examined the impact of IGF1R inhibition on cell division. We found that siRNA-mediated knockdown of IGF1R from HeLa S3 cells leads to M-phase delays. Although IGF1R depletion causes partial exclusion of FoxM1 from the nucleus, quantitative real-time PCR revealed that the transcription of M-phase regulators is not affected by decreased levels of IGF1R. Moreover, a similar delay in M phase was observed following 2 h of incubation with the IGF1R inhibitors OSI-906 and NVP-ADW742. These results suggest that the M-phase delay observed in IGF1R-compromised cells is not caused by altered expression of mitotic regulators. Live-cell imaging revealed that both prolonged prometaphase and prolonged metaphase underlie the delay and this can be abrogated by the inhibition of Mps1 with AZ3146, suggesting activation of the Spindle Assembly Checkpoint when IGF1R is inhibited. Furthermore, incubation with the Aurora B inhibitor ZM447439 potentiated the IGF1R inhibitor-induced suppression of cell proliferation, opening up new possibilities for more effective cancer chemotherapy.

Fibroblasts During Hypertrophic Scar Formation and Resolution

1973 ◽  
Vol 31 ◽  
pp. 428-429
Author(s):  
C. W. Kischer
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Cell Proliferation ◽  
Fine Structure ◽  
Metabolic Activity ◽  
Hypertrophic Scar ◽  
Normal Skin ◽  
Ground Substance ◽  
Hypertrophic Scars ◽  
Scanning Electron

The morphology of the fibroblasts changes markedly as the healing period from burn wounds progresses, through development of the hypertrophic scar, to resolution of the scar by a self-limiting process of maturation or therapeutic resolution. In addition, hypertrophic scars contain an increased cell proliferation largely made up of fibroblasts. This tremendous population of fibroblasts seems congruous with the abundance of collagen and ground substance. The fine structure of these cells should reflect some aspects of the metabolic activity necessary for production of the scar, and might presage the stage of maturation.A comparison of the fine structure of the fibroblasts from normal skin, different scar types, and granulation tissue has been made by transmission (TEM) and scanning electron microscopy (SEM).

The Effect of Androgen Depletion and Replacement on the Epithelium of the Seminal Vesicle of the Aging Rat

1975 ◽  
Vol 33 ◽  
pp. 590-591
Author(s):  
Venita F. Allison
Keyword(s):  
Cell Proliferation ◽  
Seminal Vesicle ◽  
Male Rats ◽  
Target Cells ◽  
Cell Regeneration ◽  
Secretory Function ◽  
Electron Microscopic ◽  
Aging Rat ◽  
Microscopic Studies ◽  
Androgen Depletion

In 1930, Moore, Hughes and Gallager reported that after castration seminal vesicle epithelial cell atrophy occurred and that cell regeneration could be achieved with daily injections of testis extract. Electron microscopic studies have confirmed those observations and have shown that testosterone injections restore the epithelium of the seminal vesicle in adult castrated male rats. Studies concerned with the metabolism of androgens point out that dihydrotestosterone stimulates cell proliferation and that other metabolites of testosterone probably influence secretory function in certain target cells.Although the influence of androgens on adult seminal vesicle epithelial cytology is well documented, little is known of the effect of androgen depletion and replacement on those cells in aging animals. The present study is concerned with the effect of castration and testosterone injection on the epithelium of the seminal vesicle of aging rats.

Acetaminophen: Macula densa hypersecretory activity by induced hepatotoxicity

1987 ◽  
Vol 45 ◽  
pp. 934-935
Author(s):  
S.S. Poolsawat ◽  
C.A. Huerta ◽  
S.TY. Lae ◽  
G.A. Miranda
Keyword(s):  
Cell Proliferation ◽  
Liver Function ◽  
Chronic Inflammation ◽  
Foam Cell ◽  
Term Effect ◽  
Short Term ◽  
Drug Induced ◽  
Experimental Induction ◽  
Tissue Alterations ◽  
Toxic Responses

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.

EMBJ08, a novel gene promoting cell proliferation

2010 ◽  
Vol 34 (8) ◽  
pp. S50-S50
Author(s):  
Jing Li ◽  
Dongxia Hao ◽  
Weiwei Deng ◽  
Na Li ◽  
Shai Guo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Novel Gene
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