CKS1B promotes the growth of ovarian cancer cells by regulating the expression of PD-L1

Ovarian cancer has high rates of morbidity and mortality and a poor prognosis. A growing body of research suggests that CDC28 protein kinase regulatory subunit 1B (CKS1B) influences the progression of numerous carcinomas. However, the specific mechanism of CKS1B in ovarian cancer has yet to be elucidated. Here, this study aimed to investigate the involvement of CKS1B in the progression of ovarian cancer. Initially, we collected data from the Cancer Genome Atlas (TCGA) website and ovarian cancer tissues showed elevated CKS1B expression compared to healthy tissues, indicating a poorer prognosis. Immunohistochemistry (IHC) was used to detect CKS1B and programmed cell death 1-ligand 1 (PD-L1) levels and demonstrated that CKS1B is positively related to PD-L1 expression. Then, short-interfering (si)-CKS1B or sinegative control (si-NC) constructs were transfected into SKOV3 and OVCAR3 cells. Subsequently, cell viability was measured by cell counting kit-8 (CCK8) and colony formation assays, and the extent of apoptosis was assessed using flow cytometry. We found that CKS1B silencing inhibited cell growth and promoted cell apoptosis in ovarian cancer. In addition, the expression levels of CKS1B, B-cell lymphoma-2 (BCL2)associated X (Bax), cleaved-caspase3 and PD-L1 were determined by western blotting. Furthermore, to investigate whether the inhibitory effects of si-CKS1B on ovarian cancer is related to the levels of PD-L1, we added PD-L1 to si-CKS1B transfected cells and found that cells that had been supplemented with PD-L1 exhibited an increased cell growth rate and a reduced apoptosis rate than si-CKS1B cells. Collectively, our data we demonstrated high levels of CKS1B in ovarian cancer cells, and found that the knockdown of CKS1B could alleviate the development of ovarian tumors by dysregulating the level of PD-L1 expression.