Overexpression of Aurora-A Enhances Invasion and Matrix Metalloproteinase-2 Expression in Esophageal Squamous Cell Carcinoma Cells

Wang, Xiaoxia; Lu, Na; Niu, Bo; Xian-jiu, Chen; Xie, Jun; Cheng, Niuliang

doi:10.1158/1541-7786.mcr-11-0416

Cited by 47 publications

(46 citation statements)

References 26 publications

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“…4A) and qRT-PCR (Fig. 4B) showed that the protein and mRNA expression levels of MMP-2 in Aurora-A-overexpressing cells were higher than those in the control cells, which were consistent with previous studies that knockdown of Aurora-A expression could downregulate MMP-2 expression [22,23].…”

Section: Aurora-a Overexpression Promotes Escc Cell Invasion Via Upresupporting

confidence: 90%

“…It has been shown that nuclear translocation of NF-κB is influenced by many signaling pathways, including AKT pathway [24]. Interestingly, our previous results indicated that Aurora-A overexpression increases MMP-2 expression through AKT signaling pathway [22]. Hence, to identify whether AKT pathway participates in Aurora-A-mediated NF-κB activation, AKT inhibitor was added to Aurora-A-overexpressing cells for 48 h. Western blot analysis demonstrated that inhibition of AKT significantly decreased nuclear accumulation of NF-κB in Aurora-A-overexpressing cells (Fig.…”

Section: Aurora-a Overexpression Upregulates Mmp-2 Expression Via Aktmentioning

confidence: 81%

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Aurora-A modulates MMP-2 expression via AKT/NF-κB pathway in esophageal squamous cell carcinoma cells

Wang

et al. 2016

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Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies. It is necessary to identify new markers for predicting tumor progression and therapeutic molecular targets. It has been reported that overexpressions of Aurora-A and matrix metalloproteinases 2 (MMP-2) may promote the malignant development of tumor. However, the relationship between Aurora-A and MMP-2 expression in tumor patients has not been investigated. In addition, the underlying mechanisms that Aurora-A regulates MMP-2 expression are still not fully elucidated.In this study, we demonstrated that Aurora-A and MMP-2 were overexpressed in ESCC tissues compared with paired normal adjacent tissues (P < 0.0001). Overexpression of Aurora-A was associated with the lymph node metastasis of ESCC (P = 0.01). Significantly, Aurora-A protein expression was positively correlated with MMP-2 protein expression in ESCC tissues (r = 0.66, P < 0.0001) as well as in ESCC cell lines. The level of Aurora-A expression was also positively correlated with the invasion capability of ESCC cells. Furthermore, Aurora-A overexpression significantly increased ESCC cell invasion by the upregulation of MMP-2 expression. In addition, Aurora-A overexpression promoted nuclear factor-kappaB (NF-κB) activation, and Aurora-Amediated MMP-2 upregulation was abrogated by NF-κB inhibitor. Further analysis showed that activation of NF-κB was severely attenuated by AKT inhibitor in cells overexpressing Aurora-A. Taken together, these data indicate that Aurora-A overexpression upregulates MMP-2 expression through activating AKT/NF-κB signaling pathway in ESCC cells. These findings reveal that Aurora-A may be used as an important indicator for the judgment of malignant behavior of ESCC, and may be an attractive target for cancer therapy.

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Section: Aurora-a Overexpression Promotes Escc Cell Invasion Via Upresupporting

confidence: 90%

Section: Aurora-a Overexpression Upregulates Mmp-2 Expression Via Aktmentioning

confidence: 81%

Aurora-A modulates MMP-2 expression via AKT/NF-κB pathway in esophageal squamous cell carcinoma cells

Wang

et al. 2016

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“…43 Among various growth factor-activated signaling pathways, the PI 3 K/Akt and MAPK signaling pathways have been shown to be the important growth factor-activated pathways in the tumorogenesis of many types of cancers, including HCC. 44,45 Previously, it has been reported that overexpression of Aurora A could induce the activation of PI3K/Akt and MAPK signaling pathways in human cancers. 46,47 However, whether activation of both signaling pathways mediated the downstream effects of HIF-1α and Aurora A is unclear.…”

Section: Discussionmentioning

confidence: 99%

The role of Aurora A in hypoxia-inducible factor 1α-promoting malignant phenotypes of hepatocelluar carcinoma

et al. 2013

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overexpression of both hypoxia-inducible factor 1α (HIF-1α) and aurora a has been found in hepatocelluar carcinoma (HCC). However, whether HIF-1α and aurora a synergistically promote malignant phenotypes of HCC cells is unknown. the purpose of this study was to investigate the roles and functional correlation of HIF-1α and aurora a in HCC progression. Immunohistochemistry was performed to detect HIF-1α and aurora a protein expression in 55 primary HCC and corresponding non-tumor tissues and their clinical significance. Gene knockout technology using short hairpin rNa (shrNa) was used to knockdown expression of HIF-1α or aurora a and analyze their effects on malignant phenotypes of HCC cells. the transcriptional regulation of aurora a by HIF-1α and the possible downstream molecular signaling pathways were also determined. results showed that hypoxia could induce the increased expression of HIF-1α and aurora a in HCC cells. also, shrNa-mediated HIF-1α downregulation could lead to the decreased aurora a expression and inhibition of growth or invasion in HCC cells. Moreover, HIF-1α could transcriptionally regulate aurora a expression by binding to hypoxia-responsive elements in the aurora a promoter and recruiting the coactivator-p300/ CBP. additionally, shrNa-mediated aurora a knockdown could mimic the effects of HIF-1α downregulation on phenotypes of HCC cells, and overexpression of aurora a could partially rescue the phenotypical changes of HCC cells induced by HIF-1α downregulation. Further research indicated that activation of akt and p38-MaPK signaling pathways mediated the downstream effects of HIF-1α and aurora a in HCC cells under hypoxic condition. taken together, our findings indicated that aurora a might be a key regulator of HIF-1α-promoting malignant phenotypes of HCC by activation of akt and p38-MaPK signaling pathways.

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“…The ERK/MAPK signaling pathway is known to serve important roles in the progression of cancer through affecting a number of cellular processes, including gene expression, and cell proliferation, apoptosis, migration and invasion (21,22). In the current study, a positive correlation between Igf2as expression and ERK activation was demonstrated.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA Igf2as controls hepatocellular carcinoma progression through the ERK/MAPK signaling pathway

et al. 2017

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Abstract. Long non-coding RNAs (lncRNAs) serve an important role in numerous human diseases, including cancer. Abnormal expression of lncRNAs has been associated with a number of tumor types; however, the underlying mechanisms through which lncRNA functions have yet to be elucidated. The present study primarily focuses on insulin-like growth factor 2 antisense 1 (Igf2as), a lncRNA reported to be differentially expressed in hepatocellular carcinoma (HCC). Reverse transcription-quantitative polymerase chain reaction analysis was used to determine the level of Igf2as in HCC cells and tissues. Flow cytometry was used to determine the level of cell apoptosis following Igf2as suppression and western blot analysis was used to identify altered protein expression levels. The results demonstrated that Igf2as was upregulated in HCC cells and tissues, and that the inhibition of Igf2as using a targeted small interfering RNA (si-Igf2as), significantly decreased cell proliferation and increased apoptosis. Western blot analysis identified that the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway was inhibited in cells transfected with si-Igf2as. In addition, cell migration was markedly reduced by the knockdown of Igf2as. These results suggest that lncRNA Igf2as may control hepatocellular progression primarily through the regulation of the ERK/ MAPK signaling pathway.

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Overexpression of Aurora-A Enhances Invasion and Matrix Metalloproteinase-2 Expression in Esophageal Squamous Cell Carcinoma Cells

Cited by 47 publications

References 26 publications

Aurora-A modulates MMP-2 expression via AKT/NF-κB pathway in esophageal squamous cell carcinoma cells

Aurora-A modulates MMP-2 expression via AKT/NF-κB pathway in esophageal squamous cell carcinoma cells

The role of Aurora A in hypoxia-inducible factor 1α-promoting malignant phenotypes of hepatocelluar carcinoma

Long non-coding RNA Igf2as controls hepatocellular carcinoma progression through the ERK/MAPK signaling pathway

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Overexpression of Aurora-A Enhances Invasion and Matrix Metalloproteinase-2 Expression in Esophageal Squamous Cell Carcinoma Cells

Cited by 47 publications

References 26 publications

Aurora-A modulates MMP-2 expression via AKT/NF-&kappa;B pathway in esophageal squamous cell carcinoma cells

Aurora-A modulates MMP-2 expression via AKT/NF-&kappa;B pathway in esophageal squamous cell carcinoma cells

The role of Aurora A in hypoxia-inducible factor 1α-promoting malignant phenotypes of hepatocelluar carcinoma

Long non-coding RNA Igf2as controls hepatocellular carcinoma progression through the ERK/MAPK signaling pathway

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Aurora-A modulates MMP-2 expression via AKT/NF-κB pathway in esophageal squamous cell carcinoma cells

Aurora-A modulates MMP-2 expression via AKT/NF-κB pathway in esophageal squamous cell carcinoma cells