NUSAP1 和 GTSE1 的过表达可预测 ccRCC 患者的不良预后和较短的无病生存期

Although it has been reported that NUSAP1 and GTSE1 are highly expressed in different types of tumors and associated with malignant progression and poor clinical prognosis, their significances with clinicopathological data and correlations with patients' survival in ccRCC are still poorly understood. Therefore, in our study we attempted to evaluate the link between NUSAP1 and GTSE1 in ccRCC and to correlate their immunoexpression with clinico-pathological parameters and the patients' survival to identify their significance as potential therapeutic targets, indicators for tumor progression, and patients' prognosis. METHOD: NUSAP1 and GTSE1 were examined in 100 ccRCC patients by immunohistochemistry. The association between NUSAP1 and GTSE1 immunoreactivity and clinicopathological variables were evaluated. The disease free survival (DFS) was examined by the Kaplan-Meier method. The multivariate Cox regressions was estimated to detect the prognostic role of both proteins.

We detected high NUSAP1 and GTSE1 expression in 60% and 62% of the cases, respectively. A significant association was detected between NUSAP1 and GTSE1 immunoexpression and size (p=0.007 and p=0.026, respectively), Fuhrman grade (p=0.022 and p=0.004, respectively), tumor stage (p=0.003 and p=0.019, respectively), TILs (p=0.026 and p=0.04 respectively), capsular invasion (p=0.002 and p=0.009, respectively), Distant metastasis (p=0.007 and p=0.009, respectively), and DFS (p=0.007 and 0.009, respectively). Multivariate Cox regression showed that high NUSAP1 and GTSE1 expression levels were independently associated with an unfavourable poor prognosis of ccRCC cases.

We demonstrated that NUSAP1 and GTSE1 overexpression was closely related to the poor prognostic clinicopathological features of ccRCC and predicted an unfavorable prognosis. Therefore, NUSAP1 and GTSE1 might act together as potential futuristic prognostic indicators and therapeutic targets for ccRCC patients. However, further analysis in molecular studies on larger scale are mandatory to highlight the interactive crosstalk regulatory mechanisms between both markers and their combined effect on ccRCC.