Epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy. Thus, there is an emergent need to invest a novel therapeutic for EOC. In this study, we defined ubiquitin-specific protease 14 (USP14) as a therapeutic target for EOC. Western blot was used to evaluate the expression of USP14 in nine fresh EOC tissues and three fresh normal ovarian tissues. The protein level of USP14 was higher in the cancer samples compared with that in the normal ovary tissues. Immunohistochemistry analysis was performed on formalin-fixed paraffin-embedded section of 116 cases of EOCs and indicated that USP14 was significantly associated with clinical pathologic variables. Kaplan-Meier curve showed that high expression of USP14 was related to poor prognosis of EOC patients. Starvation and re-feeding assay was used to imitate cell cycle, suggesting that USP14 played a critical role in SKOV3 cell proliferation. CCK-8 assay showed that SKOV3 cells treated with USP14-shRNA (shUSP14) grew more slowly than control group. Flow cytometry revealed that the reduced expression of USP14 induced the apoptosis of the SKOV3 EOC cells. In summary, our findings suggest that USP14 is involved in the progression of EOC and that it may be a useful target of therapy in EOC.

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The aim of this study is to investigate the potential role and prognostic significance of translationally controlled tumor protein (TCTP) in human epithelial ovarian cancer (EOC). Western blot was used to evaluate the expression of TCTP in eight fresh EOC tissues. Immunohistochemistry was performed on formalin-fixed paraffin-embedded sections of 119 cases of ovarian cancers. Kaplan-Meier method indicated the relation between TCTP and EOC patients' overall survival rate. Starvation and re-feeding was used to assess cell cycle. Knocking down of TCTP and CCK8 assay showed the role of TCTP in HO8910 cell cycle. We found that TCTP was overexpressed in carcinoma tissues compared with normal tissues. Immunohistochemistry revealed that TCTP expression was significantly associated with clinicopathologic variables. Kaplan-Meier analysis revealed that high TCTP expression was significantly related to poor prognosis of the patients. Starvation and re-feeding suggested TCTP played a critical role in HO8910 cell proliferation. Interference of TCTP and CCK8 assay showed that the TCTP-siRNA treated HO8910 cells grew more slowly than the control group. CCK-8 assays and terminal-deoxynucleoitidyl transferase mediated nick end labeling assays were also performed to demonstrate the cisplatin could inhibit the survival of HO8910 cells and promote their apoptosis. All the experiments we have done showed that TCTP could promote the progression of EOC and reduce the sensitiveness of HO8910 cells to cisplatin.

We could hypothesize that Annexin A2 acted a critical role in EOC cell proliferation, and may be used as a potential and novel therapeutic target for EOC. These data suggest that Annexin A2 may promote the progression of EOC and be a therapeutic target for EOC therapy.