Aurora C is directly associated with Survivin and required for cytokinesis

Yan, Xiaomei; Cao, Lanqing; Li, Qiang; Wu, Yanhua; Zhang, Haoxing; Saiyin, Hexige; Li, Xianghua; Zhang, Xuqing; Shi, Qinghua; Liu, Yu

doi:10.1111/j.1365-2443.2005.00863.x

Cited by 116 publications

(101 citation statements)

References 33 publications

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“…Recently, it has been demonstrated that Aurora-C is a new member of the chromosomal passenger proteins interacting, similarly to Aurora-B, with INCENP and survivin, thus contributing to the regulation of chromosome segregation and cytokinesis 22,41 . In this context, it is worthwhile to mention that Aurora-B and C share the highest degree of sequence overlap with about 83% sequence identity whereas the kinases C and A share about 71% sequence identity.…”

Section: Discussionmentioning

confidence: 99%

“…19,21 Recently, also the Aurora kinase C has been demonstrated to be a chromosomal passenger protein, colocalized and able to form a complex with Aurora-B, INCENP and survivin in mitotic cells. 22 The genes encoding the 3 Aurora kinases map into regions that are affected by chromosomal abnormalities in different cancer types, and their overexpression has been detected in several tumor cell lines. 23 Aurora-A gene lies within the human chromosome region 20q13, and it is amplified in many forms of cancer such as bladder, ovarian and, at high frequency, in colorectal tumors.…”

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confidence: 99%

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Expression of Aurora kinases in human thyroid carcinoma cell lines and tissues

Ulisse

Delcros²,

Baldini

et al. 2006

Intl Journal of Cancer

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The Aurora kinases are involved in the regulation of cell cycle progression, and alterations in their expression have been shown to associate with cell malignant transformation. In the present study, we demonstrated that human thyrocytes express all 3 Aurora kinases (A, B and C) at both protein and mRNA level and this expression is cell cycle-regulated. An increase in the protein level of the 3 kinases was found, with respect to normal human thyrocytes (HTU5), in the human cell lines derived from follicular (FTC-133), papillary (B-CPAP) and anaplastic (8305C) thyroid carcinomas, but not in cells derived from a follicular adenoma (HTU42). These observations were mirrored in RT-PCR experiments for Aurora-A and B. In contrast, Aurora-C mRNA levels were not significantly different among the different cell types analyzed, suggesting that posttranscriptional mechanism(s) modulate its expression. The expression at the protein level of all 3 Aurora kinases was significantly higher in 3 thyroid papillary carcinomas with respect to normal matched tissues obtained from the same patients. Similar modifications, at the mRNA level, could be observed in 7 papillary carcinoma tissues for Aurora-A and B, but not for Aurora-C. In conclusion, we demonstrated that normal human thyrocytes express all 3 members of the Aurora kinase family, and their expression is amplified in malignant thyroid cell lines and tissues. These results suggest that the Aurora kinases may play a relevant role in malignant thyroid cancers, and may represent a putative therapeutic target for thyroid neoplasms

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Expression of Aurora kinases in human thyroid carcinoma cell lines and tissues

Ulisse

Delcros²,

Baldini

et al. 2006

Intl Journal of Cancer

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“…Therefore, our findings provide new insight into the role of AURKA in regulating p53-dependent apoptosis and enrich existing knowledge of AURKA and p53, as previous reports have shown that AURKA regulates p53 protein levels through direct interaction and phosphorylation of p53 at phosphorylation at Ser315 17 and Ser215. 34 The p53 protein is a major regulator of apoptosis, and several cancer drugs work through induction of DNA damage and activation of p53-mediated apoptosis. 35,36 The biological outcome of p53 depends on its ability to activate its downstream proapoptotic transcription targets.…”

Section: Discussionmentioning

confidence: 99%

Frequent overexpression of Aurora Kinase A in upper gastrointestinal adenocarcinomas correlates with potent antiapoptotic functions

Dar¹,

Zaika²,

Piazuelo³

et al. 2008

Cancer

105

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BACKGROUNDUpper gastrointestinal adenocarcinomas are a common cause of cancer‐related deaths. In this study, the authors investigated the prevalence and biological significance of Aurora Kinase A (AURKA) overexpression in upper gastrointestinal adenocarcinomas.METHODSQuantitative real‐time polymerase chain reaction (qRT‐PCR) and immunohistochemical staining on tumor tissue microarrays (TMA) were used to study the expression of AURKA in upper gastrointestinal adenocarcinomas. To investigate the biological and signaling impact of AURKA, the authors used multiple in vitro assays that included 3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyltetrazolium bromide (MTT), TUNEL (terminal deoxynucleotidyl transferase–mediated nick‐end labeling), cytochrome C release, flow cytometry, luciferase reporter, and Western blot analysis.RESULTSFrequent overexpression of AURKA transcript in upper gastrointestinal adenocarcinomas was detected compared with normal samples (47%; P = .001). The immunohistochemical analysis of 130 tumors demonstrated moderate‐to‐strong immunostaining of AURKA in >50% of upper gastrointestinal adenocarcinomas. By using camptothecin as a drug‐induced apoptosis in vitro model, the authors demonstrated that the expression of AURKA provided protection against apoptosis to gastrointestinal cancer cells (AGS and RKO) (P = .006) and RIE‐1 primary intestinal epithelial cells (P = .001). The AURKA overexpression mediated an increase in phosphorylation of AKTSer473 with an increase in HDM2 level. The shRNA‐knockdown of AKT in AURKA‐overexpressing cells reversed this effect and showed a significant increase in the p53 protein level, indicating a possible nexus of AURKA/AKT/p53. Indeed, overexpression of AURKA led to a remarkable reduction in the transcription activity of p53, with subsequent reductions in transcript and protein levels of its downstream proapoptotic transcription targets (p21, BAX, NOXA, and PUMA).CONCLUSIONSStudy results indicated that AURKA provides potent antiapoptotic properties to gastrointestinal cells by regulating levels of p53 through the AKT/HDM2 axis. Cancer 2008. ©2008 American Cancer Society.

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“…The encoded protein AURKC is a member of the cell cycle regulatory serine/threonine kinases (AURK A, B and C) which are essential during the mitotic cell division. AURKC is expressed specifically in the testis [14,23] where it is involved in chromatin condensation and proper attachment of homologous chromosomes during the first meiotic division [24,16]. The two recurrent truncating mutations, frameshift c.144delC mutation and p.Y248*, are expected to have a severe impact on the protein function.…”

Section: Discussionmentioning

confidence: 99%

“…AURKC protein is the third member of the Aurora subfamily of serine/threonine protein kinases and is preferentially expressed in the testis [14][15][16]. It was demonstrated that AURKC participates in the control of microtubule-kinetochore attachment, verifying the bi-orientation of the tensions preceding chromosome segregation, thus ensuring the production of euploid gametes.…”

Section: Introductionmentioning

confidence: 99%

Macrozoospermia: screening for the homozygous c.144delC mutation in AURKC gene in infertile men and estimation of its heterozygosity frequency in the Tunisian population

Ghédir

Gribaa

Mamaï

et al. 2015

J Assist Reprod Genet

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Purpose Macrozoospermia is a rare condition of male infertility characterized by the presence of close to 100 % largeheaded multiflagellar spermatozoa. The homozygous mutation (c.144delC) in aurora kinase C gene (AURKC) has been identified as the most frequent mutation causing macrozoospermia in North African patients. The aim of this study was to evaluate the prevalence of this condition in Tunisia and estimate the frequency of c.144delC mutation among infertile and control populations. Methods Sequencing c.144delC mutation was carried out in 33 macrozoospermic patients among 6652 infertile men. Minisequencing of exon3 was performed in 250 unrelated control individuals to estimate the frequency of c.144delC heterozygosity. Results More than 80 % of macrozoospermic patients were c.144delC homozygous. The prevalence of homozygous c.144delC was 0.4 % among infertile men (27/6652). The frequency of heterozygosity was 0.4 % among controls (1/250). Surprisingly, it is five times less common than established in the general population of North Africa (2 %) or in the Moroccan population (1.7 %).Conclusions We show that this mutation is relatively less frequent in the Tunisian population than in other Maghrebian populations. The occurrence of homozygous mutation among infertile men can be attributed to the high rate of consanguinity and its impact on the expression of this autosomal recessive male infertility disorder rather than a high frequency of heterozygous carriers among the general population. This highlights the importance of the molecular analysis of AURKC mutations for infertile men with high percentage of largeheaded multiflagellar spermatozoa in order to limit unnecessary in vitro fertilization attempts for them.

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Aurora C is directly associated with Survivin and required for cytokinesis

Cited by 116 publications

References 33 publications

Expression of Aurora kinases in human thyroid carcinoma cell lines and tissues

Expression of Aurora kinases in human thyroid carcinoma cell lines and tissues

Frequent overexpression of Aurora Kinase A in upper gastrointestinal adenocarcinomas correlates with potent antiapoptotic functions

Macrozoospermia: screening for the homozygous c.144delC mutation in AURKC gene in infertile men and estimation of its heterozygosity frequency in the Tunisian population

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