Knockdown of KIF15 promotes cell apoptosis by activating crosstalk of multiple pathways in ovarian cancer: bioinformatic and experimental analysis.

Ovarian cancer (OC) is the most lethal malignancy of women. Unlimited proliferation is a fundamental feature of OC cells. The genes associated with cell proliferation may be histopathologic biomarkers and targets of anti-tumor therapeutic strategies. The present study aimed to identify proliferation-associated biomarkers with prognostic, diagnostic, and therapeutic value and reveal the underlying molecular mechanism of candidate genes involved in OC by a combination of bioinformatic and experimental methods. KIF15 was upregulated in early-stage OC tissues and could predict poor prognosis of patients of Stage I and II. The knockdown of KIF15 significantly inhibited cell proliferation, tumor formation, and growth as well as promoting apoptosis of OC cells. A combination of experimental and bioinformatic analyses revealed KIF15 knockdown promoted cell apoptosis by activating crosstalk of multiple pathways in OC. KIF15, an early-stage prognostic gene, was identified as a candidate histopathologic biomarker and therapeutic target of OC.