Aurora B: A New Prognostic Marker and Therapeutic Target in Cancer

Portella, Giuseppe; Passaro, Carmela; Chieffi, Paolo

doi:10.2174/092986711794480203

Cited by 77 publications

(87 citation statements)

References 121 publications

(185 reference statements)

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“…[42][43][44][45] A large body of literature has proven that the overexpression of Aurora kinases causes the override of mitotic checkpoints in human cancers. 12,[46][47][48][49] Given the Aurora kinases' pivotal roles in the mitotic process during cell cycle, their over-expressions in malignancies and their crosstalk with tumor suppressors and oncogenic signaling pathways, small molecules targeting the Aurora kinases have attracted intense attention in the field of tumor therapy. 19,50 VX680 is a potent and selective inhibitor that targets both the Aurora A and B kinases and has demonstrated significant potential as an anti-cancer agent.…”

Section: Discussionmentioning

confidence: 99%

The p38 MAPK inhibitor BIRB796 enhances the antitumor effects of VX680 in cervical cancer

Jin

Zhang

et al. 2016

Cancer Biology & Therapy

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VX680 is a potent and selective inhibitor that targets the Aurora kinase family. The p38 mitogen-activated protein kinase (MAPK) regulates a large number of cellular pathways and plays an important role in the regulation of cell survival and apoptosis. This study aimed to evaluate the effect of VX680 on cervical cancer cells and investigate whether the effects on apoptosis are enhanced by the ablation of p38 MAPK activation. The results suggested that VX680 inhibited the proliferation of cervical cancer cells by causing G2/M phase arrest and endoreduplication and that the apoptotic effect was attenuated by the activation of p38 MAPK. However, the addition of BIRB796, which is an important p38 MAPK inhibitor, effectively eliminated the expression of p-p38 and hence significantly enhanced the cell death induced by VX680 in vitro. Further study demonstrated that BIRB796 cooperated with VX680 to suppress cervical cancer cell growth in a mouse xenograft model. Taken together, our results demonstrated that VX680 induced cell cycle arrest and endoreduplication in human cervical cancer cells. Combined treatment with VX680 and BIRB796 synergistically inhibited tumor growth both in vitro and in vivo. Dual blockade of Aurora kinases and p38 MAPK is therefore a promising strategy for cervical cancer treatment.

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Section: Discussionmentioning

confidence: 99%

The p38 MAPK inhibitor BIRB796 enhances the antitumor effects of VX680 in cervical cancer

Jin

Zhang

et al. 2016

Cancer Biology & Therapy

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“…Aurora kinase B is a kinase responsible for histone H3 phosphorylation on Serine 10 and 28 [65]. It is a chromosomal passenger protein that plays a role in the progression of mitosis and it is essential for chromosome condensation, kinetochore functions, spindle checkpoint activation, and the completion of cytokinesis [73]. The overexpression of Aurora B has been found in some tumor types, and has been associated with a poor prognosis for cancer patients [73].…”

Section: O-glcnacylation and Histone H3mentioning

confidence: 99%

“…It is a chromosomal passenger protein that plays a role in the progression of mitosis and it is essential for chromosome condensation, kinetochore functions, spindle checkpoint activation, and the completion of cytokinesis [73]. The overexpression of Aurora B has been found in some tumor types, and has been associated with a poor prognosis for cancer patients [73]. Protein phosphatase PP1 antagonizes Aurora B function and is responsible for the removal of phosphate from histone H3 [74].…”

Section: O-glcnacylation and Histone H3mentioning

confidence: 99%

The potential role of O-GlcNAc modification in cancer epigenetics

Forma

Jóźwiak

Bryś

et al. 2014

Cellular and Molecular Biology Letters

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There is no doubt that cancer is not only a genetic disease but that it can also occur due to epigenetic abnormalities. Diet and environmental factors can alter the scope of epigenetic regulation. The results of recent studies suggest that O-GlcNAcylation, which involves the addition of N-acetylglucosamine on the serine or threonine residues of proteins, may play a key role in the regulation of the epigenome in response to the metabolic status of the cell. Two enzymes are responsible for cyclic O-GlcNAcylation: O-GlcNAc transferase (OGT), which catalyzes the addition of the GlcNAc moiety to target proteins; and O-GlcNAcase (OGA), which removes the sugar moiety from proteins. Aberrant expression of O-GlcNAc cycling enzymes, especially OGT, has been found in all studied human cancers. OGT can link the cellular metabolic state and the epigenetic status of cancer cells by interacting with and modifying many epigenetic factors, such as HCF-1, TET, mSin3A, HDAC, and BAP1. A growing body of evidence from animal model systems also suggests an important role for OGT in polycomb-dependent repression of genes activity. Moreover, O-GlcNAcylation may be a part of the histone code: O-GlcNAc residues are found on all core histones.

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“…Diagnosis is usually based on identification of histological subgroups. In last years, many potential therapeutic targets has been discovered, including SOX2, SOX17, HMGA1, and HMGA 2, Aurora B, PATZ1, GPR30 and others (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29). Promising molecules capable to selectively target neoplastic cells, that are, serine-threonine kinases, TKs, HMGAs, GPR30 antagonist, proangiogenic factors inhibitors, and micro-RNAs already under clinical evaluation will open a new scenario for TGCTs treatment.…”

mentioning

confidence: 99%

New perspective on molecular markers as promising therapeutic targets in germ cell tumors

Chieffi

2016

IRDR

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Aurora B: A New Prognostic Marker and Therapeutic Target in Cancer

Cited by 77 publications

References 121 publications

The p38 MAPK inhibitor BIRB796 enhances the antitumor effects of VX680 in cervical cancer

The p38 MAPK inhibitor BIRB796 enhances the antitumor effects of VX680 in cervical cancer

The potential role of O-GlcNAc modification in cancer epigenetics

New perspective on molecular markers as promising therapeutic targets in germ cell tumors

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