Редактирование: AURKA (раздел)

==Publications==

{{medline-entry
|title=Aurora kinase mRNA expression is reduced with increasing gestational age and in severe early onset fetal growth restriction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32452402
|abstract=Oxidative damage and biochemical ageing are implicated in placental dysfunction and potentially fetal death. Cellular senescence may play a role in the pathophysiology of fetal growth restriction ([[FGR]]) and preeclampsia (PE). Aurora kinases ([[AURKA]], B and C) are important regulators of cellular division in mitosis and meiosis with implications in cellular senescence. We aimed to investigate whether aurora kinase expression is altered with placental dysfunction or placental ageing. Placenta and blood was obtained across gestation from pregnancies complicated by PE, [[FGR]] or both PE and [[FGR]], as well as gestation-matched control samples. Expression of [[AURKA]], B and C mRNA was examined using real time qPCR in both the placenta and maternal circulation. Placental aurora kinase expression decreased as gestation progressed: [[AURKA]] and [[AURKB]] were significantly reduced at 37-40 weeks, whereas [[AURKC]] was significantly reduced at 34-37 weeks, when compared to <34 weeks. In the maternal circulation, the mRNA level of [[AURKB]] was significantly reduced at >40 weeks compared to <34 weeks gestation. A significant reduction in [[AURKC]] was seen in [[FGR]] pregnancies <34 weeks compared to gestation-matched controls. Placental AURK expression is reduced with increased gestation. Circulating [[AURKB]] mRNA reduces at >40 weeks gestation, when compared to <34 weeks. [[AURKC]] is significantly reduced in placentas from pregnancies complicated by severe early onset (<34 weeks) [[FGR]] compared with gestation-matched controls. The functional role of aurora kinase in the placenta and in gestational age warrants further investigation.

|keywords=* Aurora kinase
* Cellular senescence
* FGR
* Preeclampsia
|full-text-url=https://sci-hub.do/10.1016/j.placenta.2020.04.012
}}
{{medline-entry
|title=Differential expression of [[AURKA]]/[[PLK4]] in quiescence and senescence of osteosarcoma U2OS cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32200684
|abstract=This study aimed to identify co-expressed differentially expressed genes (DEGs) in quiescence and senescence of osteosarcoma (OS) U2OS cells and investigate their biological functions. GSE94805 from Gene Expression Omnibus database was extracted, involving 12 samples of OS U2OS cells (4 quiescence, 4 senescence, and 4 control samples). After analysis of DEGs by limma package, VENN analysis was performed to identify co-expressed DEGs in quiescence and senescent. The Cytoscape software was used to construct an interactive network of co-expressed DEGs. Finally, box-plot was drawn for the co-expressed DEGs in sub-network. Besides, the relation literatures were selected in GenCLiP database for the co-expressed DEGs. Seven hundred and forty-three DEGs (255 up-regulated genes, 488 down-regulated genes) were obtained in quiescence and 2135 DEGs (1189 up-regulated genes, 946 down-regulated genes) in senescence. Through VENN analysis, 448 DEGs (131 up-regulated genes, 317 down-regulated genes) were co-expressed in quiescent and senescence. In the co-expressed DEGs network, 896 nodes (448 nodes in quiescent, 448 nodes in senescent) were obtained. Finally, 16 co-expressed DEGs were obtained in the sub-network analysis, in which Aurora kinase A ([[AURKA]]) and polo-like kinase ([[PLK4]]) had been reported in OS. [[AURKA]] and [[PLK4]] might be the key genes in quiescence and senescence of OS U2OS cells.

|keywords=* AURKA
* Osteosarcoma
* PLK4
* quiescence
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217361
}}
{{medline-entry
|title=Silencing of [[AURKA]] augments the antitumor efficacy of the [[AURKA]] inhibitor MLN8237 on neuroblastoma cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31920463
|abstract=Aurora kinase A ([[AURKA]]) has been implicated in the regulation of cell cycle progression, mitosis and a key number of oncogenic signaling pathways in various malignancies including neuroblastoma. Small molecule inhibitors of [[AURKA]] have shown potential, but still not as good as expected effects in clinical trials. Little is known about this underlying mechanism. Here, we evaluated the inhibitory effects of [[AURKA]] inhibitor MLN8237 on neuroblastoma cells to understand the potential mechanisms responsible for tumor therapy. MLN8237 treatment on neuroblastoma cell line IMR32 was done and in vivo inhibitory effects were investigated using tumor xenograft model. Cellular senescence was evaluated by senescence-associated β-gal Staining assay. Flow cytometry was used to tested cell cycle arrest and cell apoptosis. Senescence-associated signal pathways were detected by western blot. CD133 microbeads and microsphere formation were used to separate and enrich CD133  cells. [[AURKA]] small interfering RNA transfection was carried to downregulate [[AURKA]] level. Finally, the combination of MLN8237 treatment with [[AURKA]] small interfering RNA transfection were adopted to evaluate the inhibitory effect on neuroblastoma cells. We demonstrate that MLN8237, an inhibitor of [[AURKA]], induces the neuroblastoma cell line IMR32 into cellular senescence and G2/M cell phase arrest. Inactivation of [[AURKA]] results in [[MYCN]] destabilization and inhibits cell growth in vitro and in a mouse model. Although MLN8237 inhibits [[AURKA]] kinase activity, it has almost no inhibitory effect on the [[AURKA]] protein level. By contrast, MLN8237 treatment leads to abnormal high expression of [[AURKA]] in vitro and in vivo. Knockdown of [[AURKA]] reduces cell survival. The combination of MLN8237 with [[AURKA]] small interfering RNA results in more profound inhibitory effects on neuroblastoma cell growth. Moreover, MLN8237 treatment followed by [[AURKA]] siRNA forces senescent cells into apoptosis via suppression of the Akt/Stat3 pathway. The effect of [[AURKA]]-targeted inhibition of tumor growth plays roles in both the inactivation of [[AURKA]] activity and the decrease in the [[AURKA]] protein expression level.

|keywords=* Aurora kinase A
* Cellular senescence
* MLN8237
* Neuroblastoma
* Small interfering RNA
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6947931
}}
{{medline-entry
|title=Combined therapies that induce senescence and stabilize p53 block melanoma growth and prompt antitumor immune responses.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26405565
|abstract=We recently demonstrated that dual therapy combining [[AURKA]] and [[MDM2]] antagonists is effective against melanoma in preclinical settings. Notably, besides inducing apoptosis, this regimen led to tumor senescence and stimulated the host's antitumor immune defenses. Treatments leveraging both cancer cell-intrinsic and extrinsic antitumor mechanisms can improve melanoma therapeutic outcomes.

|keywords=* Aurora kinase
* apoptosis
* melanoma
* p53
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4570092
}}