Downregulation of peroxiredoxin II suppresses the proliferation and metastasis of gastric cancer cells.

Abstract

Peroxiredoxin (Prx) II is an imperative member of the superfamily of peroxidases. It serves an essential role in scavenging organic hydroperoxide and H2O2. It is involved in the development of various malignant tumors. In order to investigate the significance of Prx II expressions level in gastric cancer (GC), downregulation of Prx II was performed to investigate its role in the proliferation and migration of gastric adenocarcinoma cells. In GC cells and 45 GC specimens, the mRNA and protein expression levels of Prx II were determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, respectively. The Prx II expression profile in another 116 GC specimens was also detected with immunohistochemistry (IHC). The changes in the proliferation and migration of MKN45 and MGC-803 cells folllowing transfection with small interfering RNA (siRNA) were detected by cell counting kit (CCK)-8, western blot analysis, and Transwell migration and invasion assays. The results revealed that the expression of Prx II in GC tissues and GC cells were significantly upregulated compared with the normal control. There was a significant association between the expression level of Prx II and various factors, including tumor size, histological differentiation, the depth of invasion, the stage of tumor-node-metastasis (TNM) and lymph node metastasis in GC (P<0.05). Survival in patients with higher Prx II expression was significantly decreased compared with those with lower Prx II expression (P<0.01). Prx II, depth of invasion, lymph node metastasis and distant metastasis were identified as independent prognosis factors of GC (P<0.05). Knockdown of Prx II significantly suppressed the proliferation and the migration of GC cells. These experiments revealed that Prx II promotes the development of GC, affecting the survival of patients with GC.