Knockdown of circ_0000372 elevates PD-L1 level through sponging miR-488-3p to restrain cell viability, motility and immune escape in gastric cancer.

Gastric cancer (GC) development is influenced by crosstalk between tumor cells and host immune elements. Circ_0000372 has potential as an oncogene. This research aimed to investigate the circ_0000372 mechanism in GC. Circ_0000372 expressions were evaluated via the GSE194384 database. The overall survival of GC patients was determined via the Kaplan-Meier Survival Curve. Gene relationships were assessed using the Chi-square test. Circ_0000372 functions in GC were evaluated with qRT-PCR, Cell Counting Kit-8 analysis, 5-ethynyl-2'-deoxyuridine analysis, Transwell, Western blot, co-culture of peripheral blood mononuclear cells (PBMCs) and GC cells, flow cytometry, and ELISA. Meanwhile, the circ_0000372 mechanism was examined by RNA pull-down, dual-luciferase reporter assay, and Spearman Correlation Analysis. Finally, the circ_0000372 impact on tumor-bearing mice was analyzed by immunohistochemistry and western blot assays. Elevated circ_0000372 levels were detected in GC. Patients with raised circ_0000372 levels had a poor prognosis. Besides, circ_0000372 expressions were interrelated to TNM stage and lymph node metastasis. Silencing circ_0000372 repressed GC cell proliferation and invasion. Silencing circ_0000372 reduced immune escape with reduced PD-L1 protein levels and increased CD8 + T cell percentage. Moreover, circ_0000372 positively regulated PD-L1 expression via miR-488-3p, and circ_0000372 knockdown restrained GC cell proliferation, invasion, and immune escape by derepressing PD-L1 via sponging miR-488-3p. The interference of circ_0000372 also reduced GC tumor formation, tumor weight, and PD-L1 level with elevated IFN-γ level in vivo. A high circ_0000372 level indicated a GC poor prognosis. Silencing circ_0000372 suppressed cell proliferation, invasion, and immune escape by derepressing PD-L1 via sponging miR-488-3p.