Effects of silenced PAR-2 on cell proliferation, invasion and metastasis of esophageal cancer

• Published in: Oncology letters Vol. 14; no. 4; pp. 4115 - 4121
• Main Authors: Chen, Jinmei, Xie, Liqun, Zheng, Yanmin, Liu, Caihong
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications UK Ltd 01.10.2017; D.A. Spandidos
• Subjects: Cell cycle; Cell division; Cell growth; Deoxyribonucleic acid; DNA; Esophageal cancer; Extracellular matrix; Growth factors; Kinases; Metastasis; Oncology; Plasmids; Proteins; Tumors; Vectors (Biology); Beijing China; United States > US; China; gene silencing; esophageal cancer; cell proliferation; invasion; protease-activated receptor-2
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2017.6711

The present study aimed to investigate the effect of protease-activated receptor 2 (PAR-2) on cell proliferation, invasion and metastasis in the esophageal EC109 cell line. Two short hairpin RNA (shRNA) expression plasmids were constructed based on the PAR-2 mRNA sequence in humans, and they were transfected into the EC109 esophageal cancer cell line, and the stable interference cell line (shRNA-PAR-2 EC109) was obtained by puromycin selection. Following transfection of PAR-2 shRNA-1, PAR-2 expression was significantly downregulated in mRNA level and protein level in EC109 cells (P<0.05). The proliferation of EC109 cells transfected with PAR-2 shRNA was significantly lower than the negative control group (P<0.05). At 24, 48 and 72 h, the ratio of proliferation inhibition was 15.92, 24.89 and 32.28%, respectively. Compared with the control group, S-phase arrest was observed in cells transfected with shRNA-PAR-2. The ratio of cells in the S phase was 32.79±4.06, 26.54±1.37 and 33.45±2.46% at 24, 48 and 72 h, respectively. For invasion, the number of invasive cells was significantly lower in shRNA-PAR2-2 cells compared with the control group (P<0.05). For metastasis assay, the number of invasive cells was significantly lower in shRNA-PAR2-2 cells compared with the control group (P<0.01). In the present study, the PAR-2 shRNA plasmid was constructed successfully, which can significantly downregulate PAR-2 expression in EC109 cells. Subsequent to silencing of PAR-2, the proliferation of EC109 cells was inhibited and the capabilities of invasion and migration were reduced. It is indicated that PAR-2 may be a potential target in esophageal cancer.