Title of article :
Expression of Opa interacting protein 5 (OIP5) is associated with tumor stage and prognosis of clear cell renal cell carcinoma
Author/Authors :
Gong، نويسنده , , Mancheng and Xu، نويسنده , , Yangyang and Dong، نويسنده , , Wenjing and Guo، نويسنده , , Guiying and Ni، نويسنده , , Wenjun and Wang، نويسنده , , Yan and Wang، نويسنده , , Yongquan and An، نويسنده , , Ruihua، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2013
Pages :
6
From page :
810
To page :
815
Abstract :
Opa interacting protein 5 (OIP5), overexpressed in some types of human cancers, has been reported to be associated with the carcinogenesis of human cancer. However, the biological function and clinical significance of OIP5 in human Clear Cell Renal Cell Carcinoma (CCRCC) remains unknown. In the present study, we found the expression of OIP5 was markedly upregulated in surgical CCRCC specimens and CCRCC cell lines. Immunohistochemical analysis revealed that paraffin-embedded archival CCRCC specimens exhibited higher levels of OIP5 expression than normal renal tissues. Further statistical analysis suggested the upregulation of OIP5 was positively correlated with the Fuhrman grade (P = 0.02), T classification (P = 0.015), N classification (P = 0.018) and clinical stage (P = 0.035). Also, patients with high OIP5 expression dramatically exhibited shorter survival time (P = 0.001). In addition, the OIP5 expression was an independent prognostic marker of overall survival of CCRCC patients in a multivariate analysis (P = 0.008). Experimentally, we demonstrated that silencing OIP5 in CCRCC cell lines by specific siRNA clearly inhibited cell growth. In conclusion, our findings suggested that OIP5 could be a valuable marker of CCRCC progression and prognosis, and a promising therapeutic target for CCRCC.
Keywords :
Opa interacting protein 5 (OIP5) , Clear cell renal cell carcinoma , RNA interference , progression , Prognosis
Journal title :
Acta Histochemica
Serial Year :
2013
Journal title :
Acta Histochemica
Record number :
1760240
Link To Document :
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