AURKA promotes cell migration and invasion of head and neck squamous cell carcinoma through regulation of the AURKA/Akt/FAK signaling pathway

Wu, Jichang; Yang, Liyun; Shan, Yijun; Cai, Changping; Wang, Shili; Zhang, Hao

doi:10.3892/ol.2016.4110

Cited by 34 publications

(25 citation statements)

References 30 publications

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“…Our findings further confirmed the association of the reduced expression of AURKA with the invasiveness of BC. Besides, AURKA phosphorylation activated the microtubule-associated oncogene known as the targeting protein for xenopus kinesin-like protein 2 (TPX2 ), which contributes to the migration and invasion of cancer cells through the Akt and focal adhesion kinase signaling (Yang et al, 2015;Wu et al, 2016). As shown in this research, the reduced expression of AURKA was detectable in the peripheral blood of cancer patients.…”

Section: Resultssupporting

confidence: 58%

Reduced expression of AURKA in peripheral blood of breast cancer patients

Goh¹,

See²,

Chua³

et al. 2018

bta

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AURKA, CENPW, and TIMP1 are reported to be genes involved in the regulation of the cell cycle and are highly associated with various cancers, including breast cancer (BC). These genes appear to be overexpressed in cancerous tissues, but unknown in peripheral blood. This study uses quantitative real-time PCR (qPCR) to assess the differential expression of AURKA, CENPW, and TIMP1 genes in the peripheral blood of BC patients and correlates expression levels with clinicopathological characteristics and etiological factors. We found that AURKA expression was significantly reduced in BC patients, as well as: 1) those without any family cancer history, 2) nonsmokers, and 3) those who engage in frequent consumption of red meat in the peripheral blood. However, all three genes in this study were not significantly correlated with clinicopathological characteristics of BC. Our study reveals that the expression of AURKA is significantly downregulated in the peripheral blood of BC patients.

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Section: Resultssupporting

confidence: 58%

Reduced expression of AURKA in peripheral blood of breast cancer patients

Goh¹,

See²,

Chua³

et al. 2018

bta

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“…AKT is activated by phosphorylation, and it is able to phosphorylate and activate downstream substrates, stimulating cell migration [ 50 ]. Besides the conventional function of AuA in the mitotic regulation of the cell cycle, the non-mitotic roles of AuA in cell migration and tumorigenesis have attracted considerable attention recently [ 16 , 36 , 51 , 52 ]. Consistent with previous reports, our study demonstrated that ARD1-mediated AuA acetylation induces the expression of phosphorylated AKT to activate cell migration, and it provides a new regulatory mechanism by which AuA facilitates cell movement.…”

Section: Discussionmentioning

confidence: 99%

ARD1-mediated aurora kinase A acetylation promotes cell proliferation and migration

Park

Seo

et al. 2017

Oncotarget

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Aurora kinase A (AuA) is a prerequisite for centrosome maturation, separation, and mitotic spindle assembly, thus, it is essential for cell cycle regulation. Overexpression of AuA is implicated in poor prognosis of many types of cancer. However, the regulatory mechanisms underlying the functions of AuA are still not fully understood. Here, we report that AuA colocalizes with arrest defective protein 1 (ARD1) acetyltransferase during cell division and cell migration. Additionally, AuA is acetylated by ARD1 at lysine residues at positions 75 and 125. The double mutations at K75/K125 abolished the kinase activity of AuA. Moreover, the double mutant AuA exhibited diminished ability to promote cell proliferation and cell migration. Mechanistic studies revealed that AuA acetylation at K75/K125 promoted cell proliferation via activation of cyclin E/CDK2 and cyclin B1. In addition, AuA acetylation stimulated cell migration by activating the p38/AKT/MMP-2 pathway. Our findings indicate that ARD1-mediated acetylation of AuA enhances cell proliferation and migration, and probably contributes to cancer development.

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“…It has been reported that the overexpression of CENPF and TOP2A is associated with poor prognosis in cancers, including HCC [49,50] . AURKA has been confirmed as an oncogene in cancer development, which promotes tumor development by promoting a variety of biological functions, including cell proliferation, migration, invasion, EMT and cancer stem cell behaviors [51,52] .…”

Section: Discussionmentioning

confidence: 99%

Identification and Analysis of the Key Genes associated with the Development from Liver Cirrhosis to Hepatocellular Carcinoma Based on Bioinformatics Analysis

Li¹,

Ding²,

Yan³

2020

Preprint

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Background: Hepatocellular carcinoma (HCC) is the most frequent primary liver tumor, and one of the most common malignant cancer with poor prognosis. Liver cirrhosis is the major risk factor for HCC. The aim of this study was to identify potential key genes associated with the development from liver cirrhosis to HCC and explore their potential mechanisms. Methods: Four microarray datasets GSE17548, GSE63898, GSE25097 and GSE89377 were downloaded from the Gene Expression Omnibus database. A protein-protein interaction (PPI) network was constructed using the STRING database, and potential hub genes were screened using MCODE plug-in in Cytoscape software. The Oncomine database was used to verify the expression of differential genes in cirrhosis and HCC. In order to further verify those hub genes, the hierarchical cluster between normal and HCC tissues was constructed using the UCSC Cancer Genomics Browser. The UALCAN database was used to verify the difference of hub genes in normal and HCC tissues and in different tumor grades. Finally, the cBioPortal online platform was used to analyze the association between the expression of hub genes and prognosis in HCC.Results: A total of 360 DEGs, including 280 downregulated and 80 upregulated genes, were identified. Gene ontology enrichment (GO) analysis showed that these DEGs were mainly enriched in monooxygenase activity, cofactor binding, and oxidoreductase activity (acting on CH-OH group of donors). The mainly enriched pathways were complement and coagulation cascades, prion diseases, and arachidonic acid metabolism. By extracting key modules from the PPI network, 16 hub genes were screened out. In the hierarchical cluster of hub genes between normal and HCC tissues, the results showed that the expression level of 16 hub genes in HCC tissues was significantly higher than that in normal tissues. In addition, expression level of the hub genes was significantly associated with the tumor grades. The survival analysis showed that six hub DEGs, including KIF20A,HMMR, RRM2, TPX2, TTK and UBE2C, were closely associated with the poor prognosis of HCC.Conclusion: Our study discovered six novel potential genes associated with the development from liver cirrhosis to HCC. These key genes may be used as prognostic biomarkers and molecular therapeutic targets for HCC.

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AURKA promotes cell migration and invasion of head and neck squamous cell carcinoma through regulation of the AURKA/Akt/FAK signaling pathway

Cited by 34 publications

References 30 publications

Reduced expression of AURKA in peripheral blood of breast cancer patients

Reduced expression of AURKA in peripheral blood of breast cancer patients

ARD1-mediated aurora kinase A acetylation promotes cell proliferation and migration

Identification and Analysis of the Key Genes associated with the Development from Liver Cirrhosis to Hepatocellular Carcinoma Based on Bioinformatics Analysis

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