SPIB Knockdown Inhibits the Immune Escape of Ovarian Cancer Cells by Reducing PD-L1 (CD274) Expression and Inactivating the JAK/STAT Pathway.

Abstract

Spi-B transcription factor (SPIB) is an E-twenty-six (ETS) transcription factor associated with tumor immunity. To investigate the functions and mechanisms of SPIB in ovarian cancer (OC) cells. Cell proliferation, apoptosis, migration, and invasion were determined using colony formation, EdU, flow cytometry, and transwell assays, respectively. The binding sites of programmed death-ligand 1 (PD-L1) and SPIB were predicted using the JASPAR database and verified using the ChIP and luciferase reporter assays. SPIB knockdown inhibited OC cell proliferation, migration, and invasion, and significantly boosted apoptosis (p<0.05). SPIB directly enhanced PD-L1 transcription in OVCAR-3 and SKOV3 cells (p<0.05). Importantly, the JAK/STAT pathway was markedly inactivated in OC cells upon SPIB knockdown. SPIB knockdown markedly decreased JAK2 and STAT1 phosphorylation in OVCAR-3 and SKOV3 cells (p<0.05). These data indicate that SPIB knockdown inhibits OC cell progression by downregulating PD-L1 and inactivating the JAK/STAT pathway.