Erschienen in:
01.10.2014 | Research Article
Enhanced expression of IMPDH2 promotes metastasis and advanced tumor progression in patients with prostate cancer
verfasst von:
L. Zhou, D. Xia, J. Zhu, Y. Chen, G. Chen, R. Mo, Y. Zeng, Q. Dai, H. He, Y. Liang, F. Jiang, W. Zhong
Erschienen in:
Clinical and Translational Oncology
|
Ausgabe 10/2014
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Abstract
Purpose
Our previous study showed the upregulation of inosine 5′-monophosphate dehydrogenase type II (IMPDH2) protein in human prostate cancer (PCa) tissues and sera compared to non-cancerous controls by proteomics and ELISA analyses. However, the clinical significance of IMPDH2 in PCa has not been fully elucidated. Thus, the aim of the current study was to investigate the associations of IMPDH2 upregulation with tumor progression in patients with PCa.
Methods
IMPDH2 expression at mRNA and protein levels in human PCa and non-cancerous prostate tissues was respectively detected by qRT-PCR, Western blot and immunohistochemistry analyses, which was validated by microarray-based Taylor Data. Then, the association of IMPDH2 expression with clinicopathological features of PCa patients was statistically analyzed.
Results
Compared with non-cancerous prostate tissues, IMPDH2 mRNA and protein expression levels were both significantly upregulated (at mRNA level: 9.22 ± 2.49 vs 5.06 ± 1.45, P < 0.01; at protein level by Western blot: 0.674 ± 0.029 vs 0.418 ± 0.140, P < 0.001; at protein level by immunohistochemistry: 4.97 ± 0.760 vs 3.32 ± 1.66, P < 0.001) in PCa tissues, which were consistent with our previous data. In addition, the enhanced expression of IMPDH2 in PCa tissues was significantly correlated with the advanced clinical stage (for our cohort: P < 0.001; for Taylor data: P = 0.002), the presence of metastasis (for our cohort: P < 0.001; for Taylor data: P = 0.012) and the higher Gleason score (for our cohort: P = 0.002; for Taylor data: P = 0.028).
Conclusions
These findings suggest for the first time that the enhanced expression of IMPDH2 may promote the tumor metastasis and the advanced tumor progression in patients with PCa.