CKS1B promotes cell proliferation and invasion by activating STAT3/PD‐L1 and phosphorylation of Akt signaling in papillary thyroid carcinoma

OBJECTIVE: To investigate role of GKS1B and its relationship between STAT3/PD‐L1 and p‐Akt in papillary thyroid carcinoma (PTC). METHODS: Expression of GKS1B and PD‐L1 was determined in PTC cell lines. GKS1B was overexpressed or knocked down by transfection with overexpression plasmids or si‐CKS1B. STAT3 inhibitor WP1066 was used to suppress STAT3, and PD‐L1 inhibitor Pembrolizumab was used to block PD‐L1. Cell viability and invasion were evaluated by MTT and transwell assay, respectively. The expression of STAT3, p‐STAT3, Akt, and p‐Akt was measured using Western blotting. RESULTS: Both protein levels and mRNA levels of CKS1B and PD‐L1 were remarkably up‐regulated in PTC cell lines. Knockdown of CKS1B significantly inhibited cell viability and invasion of PTC cells and suppressed STAT3/PD‐L1 signaling and Akt phosphorylation, while overexpression of CKS1B led to opposite results. Inhibition of STAT3 or PD‐L1 reversed the effects of overexpressed CKS1B on PTC cells. CONCLUSION: The overexpression of CSK1B could promote cell viability and invasion of PTC cells through activation of STAT3/PD‐L1 signaling and Akt phosphorylation.