Ovarian cancer is the main cause of cancer mortality in gynecological tumors around the world. Drug resistance to a variety of chemotherapeutics continue to be one of the main causes of treatment failure. In a previous study, it was demonstrated that STK17A, a proapoptotic gene, was significantly downregulated in acquired resistance phenotypes of colon cancer cells that are resistant to oxaliplatin and 5‑fluorouracil. Therefore in the present study, the association between STK17A expression and ovarian cancer with initial drug resistance was investigated and the influence of STK17 on ovarian cancer cell proliferation and doubling time. In the present study, ovarian cancer cell lines that express low levels of STK17A were established by targeting STK17A with specific siRNA. In addition, up‑regulation of STK17A was established in ovarian cells by pCDNA3flu/STK17A. The sensitivity of the transfected cells and controls to paclitaxel, carboplatin was examined by MTT assay, and the levels of proliferation and apoptosis were analyzed by flow cytometry. In the cells that were transfected with siRNA resulting in reduced expression of STK17A, the 50% inhibitory concentration (IC50) of the chemotherapy drugs paclitaxel and carboplatin was increased compared with control cells (P<0.05). By contrast, in the cells that overexpressed STK17A following treatment with pCDNA3flu/STK17A, the IC50 of the chemotherapy drugs reduced in each case, and was significantly lower compared with the control (P<0.05). There was a variable susceptibility to carboplatin and paclitaxel resulting from altering the levels of STK17A expression in ovarian cancer cell lines. The growth of STK17A/siRNA transfected cells was promoted compared with that of the control cells and accordingly their cell doubling time was shortened.

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