Aurora kinases in head and neck cancer

Mehra, Ranee; Serebriiskii, Ilya G.; Burtness, Barbara; Astsaturov, Igor; Golemis, Erica A.

doi:10.1016/s1470-2045(13)70128-1

Cited by 61 publications

(61 citation statements)

References 91 publications

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“…Interest in targeting the aurora kinases has resulted in the development of various smallmolecule inhibitors of aurora kinases A, B, or C, and panaurora inhibitors [8]. Drugs investigated in the preclinical setting included: pan-aurora kinase drugs AMG 900 and AT9283; the aurora kinase A-and B-targeted drugs barasertib (AZD1152), ZM447439, and ENMD2076; the aurorakinase-A-specific drug alisertib; and inhibitor of the aurora kinases B and C, GSK1070916A.…”

Section: Compliance With Ethical Guidelinesmentioning

confidence: 99%

“…The aurora serine/threonine kinase family in mammals includes three members (aurora kinases A, B, and C) which have key roles in the regulation of cell division, including entry into mitosis, completion of cytokinesis, and assembly of the spindle microtubules [8]. Aurora-B (Aur-B), a chromosome passenger protein, is located on the chromosome arms during prophase and at the centromeres during prometaphase and metaphase [9].…”

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confidence: 99%

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Expression of Aurora-B and FOXM1 predict poor survival in patients with nasopharyngeal carcinoma

Huang

Luo

et al. 2015

Strahlenther Onkol

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Section: Compliance With Ethical Guidelinesmentioning

confidence: 99%

mentioning

confidence: 99%

Expression of Aurora-B and FOXM1 predict poor survival in patients with nasopharyngeal carcinoma

Huang

Luo

et al. 2015

Strahlenther Onkol

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“…Squamous cell carcinomas of the head and neck are a heterogeneous group of malignancies involving the oral cavity, oropharynx, larynx and hypopharynx, and account for >90% of malignant tumors in the oral cavity (29,30). The biological properties of squamous cell carcinoma are intimately regulated by various cytokines and growth factors.…”

Section: Cxcr7 In Cancer Of the Gastrointestinal Systemmentioning

confidence: 99%

C-X-C motif receptor 7 in gastrointestinal cancer

et al. 2015

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Abstract. Chemokine receptors are key mediators of normal physiology and numerous pathological conditions, including inflammation and cancer. This receptor family is an emerging target for anticancer drug development. C-X-C motif receptor 7 (CXCR7) is an atypical chemokine receptor that was first cloned from a canine cDNA library as an orphan receptor and was initially named receptor dog cDNA 1 (RDC1). Shortly after demonstrating that RDC1 binds with its ligand, stromal cell-derived factor-1α and interferon-inducible T-cell α chemoattractant, RDC1 was officially deorphanized and renamed CXCR7, as the seventh receptor in the CXC class of the chemokine receptor family. Recent accumulating evidence has demonstrated that CXCR7 expression is augmented in the majority of tumor cells compared with their normal counterparts and is involved in cell proliferation, survival, migration, invasion and angiogenesis during the initiation and progression of breast, lung and prostate cancer. In the present review, the expression and role of CXCR7, as well as its clinical relevance in cancer of the gastrointestinal system, were investigated. In addition, the potential of this chemokine receptor as a therapeutic target in the treatment of gastrointestinal cancer was discussed.

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“…AURKB appears in the nucleus at the initial synthesis phase, and is involved in the regulation of cytokinesis by binding to several proteins containing the inhibitor Survivin (4,5). It has been reported that AURKs are overexpressed in tumor cells and, therefore, they are thought to be potential molecular targets for the treatment of malignant tumors (6)(7)(8)(9). A number of inhibitors of AURK (ZM447439, VX-680, AT9283, AZD1152, MLN8054 and MLN8237) have been developed (6).…”

Section: Introductionmentioning

confidence: 99%

In vitro evaluation of a combination treatment involving anticancer agents and an aurora kinase B inhibitor

et al. 2016

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Abstract. Aurora kinase B (AURKB) inhibitors are regarded as potential molecular-targeting drugs for cancer therapy. The present study evaluated the cytotoxic effect of a combination of AZD1152-hQPA, an AURKB inhibitor, and various anticancer agents on the HeLa human cervical cancer cell line, as well as its cisplatin-resistant equivalent HCP4 cell line. It was demonstrated that AZD1152-hQPA had an antagonistic effect on the cytotoxicity of cisplatin, etoposide and doxorubicin, but had a synergistic effect on that of all-trans-retinoic acid (ATRA), Am80 and TAC-101, when tested on HeLa cells. Cisplatin, etoposide and doxorubicin were shown to increase the cellular expression of AURKB, while ATRA, Am80 and TAC-101 downregulated its expression. These results suggested that AURKB expression is regulated by these anticancer agents at the transcriptional level, and that the level of expression of AURKB may influence the cytotoxic effect of AZD1152-hQPA. Therefore, when using anticancer agents, decreasing the expression of AURKB using a molecular-targeting drug may be an optimal therapeutic strategy. IntroductionThe human aurora kinase (AURK) family consists of three genes, including AURKA, AURKB and AURKC. Their gene products are located in different parts of the nucleus and have been suggested to function independently during the mitotic phase (M-phase) of the cell cycle (1-3). AURKB appears in the nucleus at the initial synthesis phase, and is involved in the regulation of cytokinesis by binding to several proteins containing the inhibitor Survivin (4,5). It has been reported that AURKs are overexpressed in tumor cells and, therefore, they are thought to be potential molecular targets for the treatment of malignant tumors (6-9). A number of inhibitors of AURK (ZM447439, VX-680, AT9283, AZD1152, MLN8054 and MLN8237) have been developed (6). These agents inhibit AURKA and AURKB to varying degrees, and some are currently in phase I clinical trials (10). The previously described inhibitor AZD1152 is a prodrug that changes to the active form AZD1152-hQPA in the cytoplasm, which has a dominant effect on AURKB (11).Chemotherapy using anticancer drugs, such as platinum-based therapies or taxanes, and radiotherapy are the most commonly employed strategies for the treatment of gynecological malignant tumors (12,13). AURK inhibitors are thought to be an effective molecular-targeting drug for gynecological malignant tumors (6), and clinical trials for their use against leukemia and other cancers are underway (10). In the future, there is a possibility that ARUK inhibitors may be used in combination with anticancer agents. However, it is unknown which anticancer agents would function most effectively in combination with AURK inhibitors. Sun et al (14) reported that the AURKB inhibitor, VX-680, downregulated nuclear factor (NF)-κB expression and increased the sensitivity of tumor cells to anticancer agents. Therefore, evaluation of the cellular expression or activity of NF-κB may emerge as an important basis for the use of AURK...

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Aurora kinases in head and neck cancer

Cited by 61 publications

References 91 publications

Expression of Aurora-B and FOXM1 predict poor survival in patients with nasopharyngeal carcinoma

Expression of Aurora-B and FOXM1 predict poor survival in patients with nasopharyngeal carcinoma

C-X-C motif receptor 7 in gastrointestinal cancer

In vitro evaluation of a combination treatment involving anticancer agents and an aurora kinase B inhibitor

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