Analysis of Aurora B kinase in non-Hodgkin lymphoma

Ikezoe, Takayuki; Takeuchi, Tamotsu; Yang, Jing; Adachi, Yoshihiro; Nishioka, Chie; Furihata, Mutsuo; Koeffler, H. Phillip; Yokoyama, Akihito

doi:10.1038/labinvest.2009.106

Cited by 37 publications

(32 citation statements)

References 33 publications

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“…11 The effects of AZD1152 on leuke- AZD1152 has also been shown to induce growth arrest and apoptosis in Burkitt lymphoma cell lines. 31 Several promising drug combinations are also emerging. AZD1152 increases radiosensitivity in vivo and this effect is p53-and cell cycledependent.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Aurora kinase inhibitor AZD1152 negatively affects the growth and survival of HTLV‐1‐infected T lymphocytes in vitro

Tomita

Tanaka

Mori

2010

Intl Journal of Cancer

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Aurora kinases play an essential role in regulating mitosis and cell division. Inhibition of Aurora kinases results in suppression of cell division, phosphorylation of histone H3 and induction of apoptosis in many cell types. These characteristics have prompted the testing of Aurora kinase inhibitors as chemotherapeutic agents. In our study, we report the in vitro activities of AZD1152, a selective inhibitor of Aurora B kinase in human T-cell leukemia virus type 1 (HTLV-1), the causative agent of adult T-cell leukemia (ATL), -infected T-cell lines. Overexpression of Aurora B was noted in HTLV-1-infected T-cell lines compared to HTLV-1-uninfected T-cell lines. AZD1152 reduced the viability of HTLV-1-infected T-cell lines within 24 hr but did not affect that of -uninfected T-cell lines. Although AZD1152 inhibited phosphorylation of histone H3 on Ser10 in both HTLV-1-infected and -uninfected T-cell lines, it induced polyploidy only in HTLV-1-uninfected T-cell lines. AZD1152 induced early apoptosis of HTLV-1-infected T-cells without induction of polyploidy. We have reported previously that a panAurora kinase inhibitor induced apoptosis through inhibition of NF-jB signaling activity in HTLV-1-infected T-cell lines. In contrast, AZD1152 did not affect NF-jB activity in these cells. It induced p53 and p21 expression in HTLV-1-infected but not in HTLV-1-uninfected T-cell lines, suggesting that activation of p53-dependent postmitotic checkpoint might prevent polyploidy in HTLV-1-infected T-cells. Our results suggest that specific inhibition of Aurora B kinase is a potentially useful therapeutic strategy in the treatment of ATL and that further in vivo exploration is warranted.

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Section: Discussionmentioning

confidence: 99%

Retracted: Aurora kinase inhibitor AZD1152 negatively affects the growth and survival of HTLV‐1‐infected T lymphocytes in vitro

Tomita

Tanaka

Mori

2010

Intl Journal of Cancer

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“…For histological analysis in Matrigel plugs, immunohistochemical staining of CD31was performed with a Ventana DISCOVERYTM autostainer system (Ventana Japan, Osaka, Japan) as described previously. 19 Anti-mouse CD31 antibody (Santa Cruz Biotechnology) was used. The same specimens were used for hematoxylin and eosin staining.…”

Section: Murine Angiogenesis Assaymentioning

confidence: 99%

Thrombomodulin Protects Endothelial Cells From a Calcineurin Inhibitor–Induced Cytotoxicity by Upregulation of Extracellular Signal–Regulated Kinase/Myeloid Leukemia Cell-1 Signaling

Ikezoe

Yang

Nishioka

et al. 2012

ATVB

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Objective— We have recently reported that recombinant human soluble thrombomodulin (rTM) counteracted capillary leakage associated with engraftment, as well as sinusoidal obstructive syndrome after hematopoietic stem cell transplantation. These observations prompted us to explore whether rTM possessed cytoprotective effects on endothelial cells. Methods and Results— Exposure of human umbilical vein endothelial cells to rTM induced expression of antiapoptotic protein myeloid leukemia cell-1 through the activation of extracellular signal–regulated kinase in these cells. Additional studies found that exposure of human umbilical vein endothelial cells to cyclosporine A and FK506, an immunosuppressant used for the individuals receiving hematopoietic stem cell transplantation, induced apoptosis, which was attenuated when human umbilical vein endothelial cells were exposed to these agents in the presence of rTM. Further studies using deletion mutants of thrombomodulin (TM) identified that the epidermal growth factor domain of TM possessed cytoprotective effects. A single nucleotide substitution at codon 376 or 424 of TM, which impairs the ability of TM to produce activated protein C or bind to thrombin, respectively, did not hamper the cytoprotective effects of TM, which suggested that cytoprotective effects of rTM were distinctive from those of activated protein C. Conclusion— TM may be useful for prevention, as well as treatment of endothelial cell damage after hematopoietic stem cell transplantation.

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“…34,35 To determine if CA46 and DG75 cells were also resistant to Aurora kinase inhibitors, we treated the Burkitt lymphoma cell lines for 48 h with 250 nM tozasertib or alisertib or 1 μM ZM447439 and examined cellular apoptosis by annexin V and PI staining. As shown in Figure 3, Ramos and ST486 cells readily underwent apoptosis, while CA46 and DG75 cells were nearly completely resistant to Aurora kinase inhibitor-mediated apoptosis.…”

Section: Aurora Kinase Inhibitors Are Variably Effective In Burkitt Lmentioning

confidence: 99%

Loss of the proteins Bak and Bax prevents apoptosis mediated by histone deacetylase inhibitors

Ieranò¹,

Chakraborty²,

Nicolae³

et al. 2013

Cell Cycle

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Analysis of Aurora B kinase in non-Hodgkin lymphoma

Cited by 37 publications

References 33 publications

Retracted: Aurora kinase inhibitor AZD1152 negatively affects the growth and survival of HTLV‐1‐infected T lymphocytes in vitro

Retracted: Aurora kinase inhibitor AZD1152 negatively affects the growth and survival of HTLV‐1‐infected T lymphocytes in vitro

Thrombomodulin Protects Endothelial Cells From a Calcineurin Inhibitor–Induced Cytotoxicity by Upregulation of Extracellular Signal–Regulated Kinase/Myeloid Leukemia Cell-1 Signaling

Loss of the proteins Bak and Bax prevents apoptosis mediated by histone deacetylase inhibitors

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