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Deregulation of manganese superoxide dismutase (SOD2) expression and lymph node metastasis in tongue squamous cell carcinoma

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posted on 12.05.2011, 00:00 authored by Xiqiang Liu, Anxun Wang, Lorenzo L. Muzio, Antonia Kolokythas, Shihu Sheng, Corrado Rubini, Hui Ye, Fei Shi, Tianwei Yu, David L. Crowe, Xiofeng Zhou
Background: Lymph node metastasis is a critical event in the progression of tongue squamous cell carcinoma (TSCC). The identification of biomarkers associated with the metastatic process would provide critical prognostic information to facilitate clinical decision making. Previous studies showed that deregulation of manganese superoxide dismutase (SOD2) expression is a frequent event in TSCC and may be associated with enhanced cell invasion. The purpose of this study is to further evaluate whether the expression level of SOD2 is correlated with the metastatic status in TSCC patients. Methods: We first examined the SOD2 expression at mRNA level on 53 TSCC and 22 normal control samples based on pooled-analysis of existing microarray datasets. To confirm our observations, we examined the expression of SOD2 at protein level on an additional TSCC patient cohort (n = 100), as well as 31 premalignant dysplasias, 15 normal tongue mucosa, and 32 lymph node metastatic diseases by immunohistochemistry (IHC). Results: The SOD2 mRNA level in primary TSCC tissue is reversely correlated with lymph node metastasis in the first TSCC patient cohort. The SOD2 protein level in primary TSCC tissue is also reversely correlated with lymph node metastasis in the second TSCC patient cohort. Deregulation of SOD2 expression is a common event in TSCC and appears to be associated with disease progression. Statistical analysis revealed that the reduced SOD2 expression in primary tumor tissue is associated with lymph node metastasis in both TSCC patient cohorts examined. Conclusions: Our study suggested that the deregulation of SOD2 in TSCC has potential predictive values for lymph node metastasis, and may serve as a therapeutic target for patients at risk of metastasis.

Funding

This work was supported in part by NIH PHS grants CA135992, CA139596, DE014847, a grant from Prevent Cancer Foundation (to X.Z.), and a Science and Technique grant (2004B30901002) from Guangdong, China (to A.W.). X.L. is supported in part by grants from the National Natural Science Foundation (30700952), and the Natural Science Foundation of Guangdong (06300660), China.

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Publisher Statement

The original version is available through BioMed Central at DOI: 10.1186/1471-2407-10-365. © 2010 Liu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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BioMed Central

Language

en_US

issn

1471-2407

Issue date

09/07/2010

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