Targeting Aurora kinase A suppresses the growth of human oral squamous cell carcinoma cells in vitro and in vivo

Tanaka, Hiroshi; Nakashiro, Koh‐ichi; Iwamoto, Kazuki; Tokuzen, Norihiko; Fujita, Yohei; Shirakawa, Rikimaru; Oka, Ryota; Goda, Hiroyuki; Hamakawa, Hiroyuki

doi:10.1016/j.oraloncology.2013.02.002

Cited by 19 publications

(20 citation statements)

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“…Furthermore, AURKA depletion significantly increased the cytotoxicity of paclitaxel (54). The suppressive effect of AURKA depletion on tumor growth was also confirmed by Tanaka et al (60), who demonstrated that AURKA plays a pivotal role in the growth of human OSCC cells, and that AURKA silencing appears to be a potentially useful therapeutic approach for patients with OSCC.…”

Section: Aurka Inhibition and Paclitaxel As Targeted Combination Thermentioning

confidence: 53%

“…Aurora kinase A (AURKA) is a member of the conserved serine/threonine protein kinase family, and a cell cycle-regulated kinase involved in spindle formation and chromosome segregation (54–60). It was observed that AURKA overexpression induces oncogenic transformation accompanied by centrosome amplification and aneuploidy in rodent cells (55,56).…”

Section: Aurka Inhibition and Paclitaxel As Targeted Combination Thermentioning

confidence: 99%

“…Furthermore, the AURKA gene is amplified and overexpressed in numerous human cancers, including breast, bladder, colorectal, ovarian gastric and pancreatic cancer, causing resistance to paclitaxel (Taxol) (54). A correlation between AURKA mRNA overexpression, tumor progression and shortened survival in patients with HNSCC was determined (54–60). …”

Section: Aurka Inhibition and Paclitaxel As Targeted Combination Thermentioning

confidence: 99%

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RNA interference in head and neck oncology

2016

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Head and neck squamous cell carcinoma (HNSCC) is the sixth leading cause of cancer worldwide. The treatment of choice in case of head and neck cancer is surgery, followed by chemo- or/and radiotherapy. A potentially effective instrument to improve the outcome of numerous diseases, including viral infections, diabetes and cancer, is RNA interference (RNAi). It has been demonstrated that small interfering RNA and microRNA molecules are strongly involved in the regulation of various different pathological processes in cancer development. RNAi has become a valuable research tool allowing a better understanding of the mechanisms regulating cancer pathogenesis. Considering those advantages over other current therapeutics (including specificity and high efficacy), RNAi appears to be a potentially useful tool in cancer treatment. The present review discusses the current knowledge about the possibility of using RNAi in HNSCC therapy.

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Section: Aurka Inhibition and Paclitaxel As Targeted Combination Thermentioning

confidence: 53%

Section: Aurka Inhibition and Paclitaxel As Targeted Combination Thermentioning

confidence: 99%

Section: Aurka Inhibition and Paclitaxel As Targeted Combination Thermentioning

confidence: 99%

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RNA interference in head and neck oncology

2016

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“…Survivin expression in premalignant oral lesions that progressed to SCC was significantly higher than that in premalignant lesions that did not progress. Moreover, in relation to the pathogenesis of this type of neoplasm, it is associated with aggressiveness, dissemination, and disease recurrence (Khan, Vaishali, & Sharma, 2010;Lin, Hung, Kuo, Chiang, & Kuo, 2005;Tanaka et al, 2013). Lauxen et al (2014) reported positive immunostaining for survivin in all SCCs.…”

Section: Discussionmentioning

confidence: 99%

Predictive value of p63, ki‐67, and survivin expression in oral leukoplakia: A tissue microarray study

Dias

Flores

Oliveira

et al. 2017

Microscopy Res & Technique

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The aim of this study was to analyze the immunohistochemical expression of survivin, ki-67, and p63 in oral leukoplakic lesions, histopathologically differentiated into dysplastic and nondysplastic. A tissue microarray containing 57 samples of biopsies from clinically classified lesions, such as leukoplakia, was immunolabeled for survivin, ki-67, and p63. Samples were scored for percentage of positively stained. Scores were designated as follows: low = less than 25% of positive cells; and high = more than 25% of positive cells. On performing histopathological diagnosis, 20 dysplastic lesions and 37 nondysplastic lesions were seen, in which female patients (56.1%) were predominant with an average age of 58.27 years. The study showed a high expression of 37.5% for survivin, 43.7% for ki-67, and 88.2% for p63 in dysplastic lesions. However, there was a high expression of 16.7% for survivin, 16.7% for ki-67, and 92% for p63 in nondysplastic lesions. There is a positive correlation of expression among the three antibodies. In the association of immunoreactivity, in both dysplastic and nondysplastic lesions, increased expression of survivin reflects on the increased expression of ki-67, and there is an overexpression of p63. In leukoplakia, the expression of survivin associated with that of ki-67 reinforces the assumption that all these lesions are potentially malignant, regardless of histopathology; and the overexpression of p63 may indicate carcinogenic potential. These findings may help in the treatment of patients with this type of lesion.

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“…12 Targeting AURKA suppresses the growth of human oral squamous cell Gene MCM2 RFC4 FEN1 RRM2 MCM6 TOP2A AURKA MCM5 CDC6 CCNB1 MCM4 EZH2 TMPO CCNA2 RFC3 MCM3 RRM1 CENPA MCM7 MAD2L1 BUB1B KIF11 CHEK1 BRCA1 CCNE1 POLE2 carcinoma cells in vitro and in vivo. 13 A specific AURKA inhibitor (MLN8237) is currently tested in clinical trials in patients with advanced malignancies, and preclinical results suggest that this might also be a promising novel targeted therapy in multiple myeloma. 14 Furthermore, AURKA is associated with worse prognosis in estrogen receptor positive breast carcinomas.…”

Section: Discussionmentioning

confidence: 99%

Expression profiling of metastatic renal cell carcinoma using gene set enrichment analysis

et al. 2013

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Abbreviations & Acronyms AURKA = aurora-kinase A ES = enrichment score FEN1 = flap structure-specific endonuclease 1 G1 = low grade G3 = high grade GSEA = gene set enrichment analysis RCC = renal cell carcinoma Objective: To identify complex changes in cell biology occurring during metastatic progression of renal cell carcinoma using a novel gene expression analysis algorithm. Methods: Whole genome expression profiling was carried out on 32 snap-frozen samples of clear-cell renal cell carcinoma metastases, 29 primary tumors (14 low grade, 15 high grade) and 14 samples of normal kidney tissue using oligonucleotide microarrays. These data were analyzed with the gene set enrichment analysis method, which is able to detect even small, but significant, expression changes in functionally connected genes that cannot be shown by gene-by-gene comparisons. Results: There were 95 gene sets (pathways) with significant upregulation in metastases compared with normal kidney tissue (P < 0.01), and 77 gene sets with significant downregulation, respectively. Low-grade and high-grade tumors showed deregulation of various pathways that have previously not been described in renal cell carcinoma. There were significant changes of genes involved in cell cycle control, apoptosis, cell motility, metabolism, cell adhesion and cytoskeleton. Some promising new potential therapy targets were identified in renal cell carcinoma metastases; for example, aurora-kinase A and flap structurespecific endonuclease 1. Conclusion: Expression profiling of metastatic renal cell carcinoma using the gene set enrichment analysis pathway analysis method provides new and detailed insights in alterations occurring in renal cell carcinoma during malignant transformation and progression. These data can help to develop new and specifically targeted renal cell carcinoma therapies.

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Targeting Aurora kinase A suppresses the growth of human oral squamous cell carcinoma cells in vitro and in vivo

Cited by 19 publications

References 29 publications

RNA interference in head and neck oncology

RNA interference in head and neck oncology

Predictive value of p63, ki‐67, and survivin expression in oral leukoplakia: A tissue microarray study

Expression profiling of metastatic renal cell carcinoma using gene set enrichment analysis

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