Elevated linc00936 or silenced microRNA-425-3p inhibits immune escape of gastric cancer cells via elevation of ZC3H12A.

Abstract Objective Gastric cancer (GC) is a malignant tumor originated from gastric mucosa. Without effective therapy, this study was to investigate the mechanism of long intergenic noncoding RNA 00936 (linc00936)/microRNA-425-3p (miR-425-3p)/monocyte chemotactic protein-induced protein 1 (ZC3H12A) axis mediating immune escape of GC cells. Methods Peripheral blood samples, GC tissues and adjacent tissues were collected. The levels of CD3+, CD4+, and CD8+ in peripheral blood were detected. The expression levels of linc00936, miR-425-3p and ZC3H12A in GC tissues and cells were detected. The correlation between the expression of linc00936 in the tissues and the levels of CD3+, CD4+ and CD8+ in the peripheral blood of GC patients was analyzed. Cytokine-induced killer (CIK) cells were induced, and co-incubated with GC cells. BGC-823 and MKN-45 cells were screened and transfected with linc00936- or miR-425-3p-related oligonucleotides to figure out their roles in immune escape, migration, apoptosis and the cytotoxicity of CIK cells in GC cells. Results Elevated miR-425-3p and reduced linc00936, and ZC3H12A expression levels were found in GC tissues and cells. Linc00936 expression was positively correlated with CD3+ and CD4+, and negatively correlated with CD8+ in peripheral blood of patients with GC. Up-regulating linc00936 or down-regulating miR-425-3p inhibited immune escape, migration, promoted apoptosis of GC cells, as well induced CIK cell cytotoxicity to GC cells. Down-regulated linc00936 or elevated miR-425-3p facilitated immune escape, migration, depressed apoptosis of GC cells, and reduced the cytotoxicity of CIK cells to GC cells. Conclusion The study concludes that up-regulated linc00936 or silenced miR-425-3p inhibits immune escape of GC cells via elevation of ZC3H12A.