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Journal of Zhejiang University SCIENCE B

ISSN 1673-1581(Print), 1862-1783(Online), Monthly

DcR3 and survivin are highly expressed in colorectal carcinoma and closely correlated to its clinicopathologic parameters

Abstract: Objective: To investigate the expression of death decoy receptor 3 (DcR3) and survivin in colorectal carcinoma. Methods: Tumor and normal tissues were taken from a total of 100 colorectal carcinoma patients during surgery, and the expression of DcR3 and survivin was examined by immunohistochemistry, Western blotting, and reverse transcription-polymerase chain reaction (RT-PCR) analyses. Results: RT-PCR showed that the expression levels of DcR3 mRNA (0.846±0.242, P<0.01) and survivin mRNA (0.7835±0.2392, P<0.01) in colorectal cancer tissues were significantly higher than those in adjacent normal tissues. Western blotting showed that the expression levels of DcR3 protein (0.795±0.261, P<0.01) and survivin protein (0.6765±0.1351, P<0.01) in tumor tissues were significantly higher than those in non-cancer tissues. The immunohistochemical streptavidin-peroxidase (SP) method showed that the positive expression rates of DcR3 and survivin were 67.0% and 58.0% in colorectal cancer tissues, and 18.0% and 3.0% in non-cancerous colorectal tissues (P<0.05), respectively. The positive correlations of DcR3 (P<0.01) and survivin (P<0.01) to the differentiation of colorectal carcinoma cells, lymph node metastasis, and pathological stage were observed. The expression of DcR3 and survivin was found to be positively correlated to clinicopathologic parameters of colorectal carcinoma. Conclusion: The overexpressed DcR3 and survivin in colorectal cancer may contribute to the development of the cancer. The monitoring of these two proteins may be useful for the diagnosis, differentiation, metastasis, and determination of stages of colorectal carcinoma.

Key words: Death decoy receptor 3 (DcR3), Survivin, Colorectal carcinoma


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DOI:

10.1631/jzus.B0920077

CLC number:

R735

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Received:

2009-03-03

Revision Accepted:

2009-07-31

Crosschecked:

2009-08-18

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