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Overexpression of Aurora-A promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability

The purpose of the study was to investigate the expression of Aurora-A in human laryngeal squamous cell carcinoma (LSCC) and to explore the effects of Aurora-A silencing on invasion and chromosomal instability in laryngeal cancer HEp-2 cells. The expression of Aurora-A mRNA and protein were studied...

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Autores principales: Zhang, Hao, Chen, Xuehua, Jin, Yuesheng, Liu, Bingya, Zhou, Liang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259349/
https://www.ncbi.nlm.nih.gov/pubmed/21584819
http://dx.doi.org/10.1007/s00405-011-1629-4
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author Zhang, Hao
Chen, Xuehua
Jin, Yuesheng
Liu, Bingya
Zhou, Liang
author_facet Zhang, Hao
Chen, Xuehua
Jin, Yuesheng
Liu, Bingya
Zhou, Liang
author_sort Zhang, Hao
collection PubMed
description The purpose of the study was to investigate the expression of Aurora-A in human laryngeal squamous cell carcinoma (LSCC) and to explore the effects of Aurora-A silencing on invasion and chromosomal instability in laryngeal cancer HEp-2 cells. The expression of Aurora-A mRNA and protein were studied using reverse transcription-PCR and Western blot in LSCC tissues and corresponding normal epithelium, respectively. In addition, the correlation between Aurora-A expression and clinicopathologic characteristics was analyzed in LSCC patients. Furthermore, HEp-2 cells were transfected with Aurora-A short hairpin RNA and the effects of knockdown of Aurora-A on tumor invasion and chromosomal instability were investigated. The results showed that expression of Aurora-A mRNA was significantly upregulated in laryngeal tumor tissue compared with that in normal tissue (P = 0.001), and overexpression of Aurora-A was found in 64.0% (16 of 25) of the patients by Western blotting. Upregulation of Aurora-A mRNA was significantly correlated with regional lymph node metastasis (P = 0.007) and clinical stage III/IV (P = 0.022). Overexpression of Aurora-A was significantly associated with lymph node metastasis (P = 0.027). Furthermore, disruption of Aurora-A using RNA interference technique suppressed invasive ability and chromosomal instability in HEp-2 cells. In conclusion, Aurora-A expression is elevated in human LSCC and associated with regional lymph node metastasis and late clinical stage. Overexpression of Aurora-A may contribute to LSCC carcinogenesis and progression partially due to enhancement of invasion ability and chromosomal instability.
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spelling pubmed-32593492012-01-31 Overexpression of Aurora-A promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability Zhang, Hao Chen, Xuehua Jin, Yuesheng Liu, Bingya Zhou, Liang Eur Arch Otorhinolaryngol Head and Neck The purpose of the study was to investigate the expression of Aurora-A in human laryngeal squamous cell carcinoma (LSCC) and to explore the effects of Aurora-A silencing on invasion and chromosomal instability in laryngeal cancer HEp-2 cells. The expression of Aurora-A mRNA and protein were studied using reverse transcription-PCR and Western blot in LSCC tissues and corresponding normal epithelium, respectively. In addition, the correlation between Aurora-A expression and clinicopathologic characteristics was analyzed in LSCC patients. Furthermore, HEp-2 cells were transfected with Aurora-A short hairpin RNA and the effects of knockdown of Aurora-A on tumor invasion and chromosomal instability were investigated. The results showed that expression of Aurora-A mRNA was significantly upregulated in laryngeal tumor tissue compared with that in normal tissue (P = 0.001), and overexpression of Aurora-A was found in 64.0% (16 of 25) of the patients by Western blotting. Upregulation of Aurora-A mRNA was significantly correlated with regional lymph node metastasis (P = 0.007) and clinical stage III/IV (P = 0.022). Overexpression of Aurora-A was significantly associated with lymph node metastasis (P = 0.027). Furthermore, disruption of Aurora-A using RNA interference technique suppressed invasive ability and chromosomal instability in HEp-2 cells. In conclusion, Aurora-A expression is elevated in human LSCC and associated with regional lymph node metastasis and late clinical stage. Overexpression of Aurora-A may contribute to LSCC carcinogenesis and progression partially due to enhancement of invasion ability and chromosomal instability. Springer-Verlag 2011-05-17 2012 /pmc/articles/PMC3259349/ /pubmed/21584819 http://dx.doi.org/10.1007/s00405-011-1629-4 Text en © The Author(s) 2011 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Head and Neck
Zhang, Hao
Chen, Xuehua
Jin, Yuesheng
Liu, Bingya
Zhou, Liang
Overexpression of Aurora-A promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability
title Overexpression of Aurora-A promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability
title_full Overexpression of Aurora-A promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability
title_fullStr Overexpression of Aurora-A promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability
title_full_unstemmed Overexpression of Aurora-A promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability
title_short Overexpression of Aurora-A promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability
title_sort overexpression of aurora-a promotes laryngeal cancer progression by enhancing invasive ability and chromosomal instability
topic Head and Neck
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259349/
https://www.ncbi.nlm.nih.gov/pubmed/21584819
http://dx.doi.org/10.1007/s00405-011-1629-4
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