Increased expression of protein kinase CK2? correlates with poor patient prognosis in epithelial ovarian cancer.
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ABSTRACT: Epithelial ovarian cancer (EOC) is one of the deadly gynecological malignancies. The function of protein kinase CK2? (CK2?) in EOC is still unknown. Our study aimed to investigate the relationship between the protein expression of CK2? and the tumor progression, the prognosis of human EOC. In this study, we analyzed the expression levels of CK2? through Western blot, using EOC cell lines like A2780, HO8910, COV644, OVCAR3, SKOV3, and the primary normal ovarian surface epithelial (NOSE) cells. Furthermore, OVCAR3 and SKOV3 EOC cells were employed as a cellular model to study the role of CK2? on cell growth, migration, invasion, apoptosis, and cell cycle distribution. In addition, we investigated CK2? protein expression in tumor tissues from patients with EOC by immunohistochemistry and analyzed the association between CK2? expression and clinicopathologic parameters and prognosis of EOC patients. And we found that compared with NOSE cells, CK2? protein expression was increased in A2780, HO8910, OVCAR3, and SKOV3 ovarian cancer cell lines. Decreased CK2? expression suppressed OVCAR3 and SKOV3 cell growth and induced more apoptosis. CK2? knockdown using specific siRNAs inhibited migration and invasion ability of OVCAR3 and SKOV3 cells. In addition, high CK2? protein expression was found in 68.4% (80/117) of EOC patients. Increased CK2? expression of was significantly correlated with FIGO staging and peritoneal cytology. Patients with higher CK2? expression had a significantly poorer overall survival compared with those with lower CK2? expression. Multi-variate Cox regression analysis proved that increased CK2? expression was an independent prognostic marker for EOC. Taken together, our data displayed that CK2? may play a role in tumor aggressive behavior of EOC and could be used as a marker for predicting prognosis of EOC patient. High CK2? expression might predict poor patient survival.
SUBMITTER: Ma Z
PROVIDER: S-EPMC5371331 | biostudies-literature | 2017
REPOSITORIES: biostudies-literature
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