High-pressure artificial pneumothorax promotes invasion and metastasis of oesophageal cancer cells.

OBJECTIVES

This study aimed to investigate the viability, apoptosis, invasion and metastasis of oesophageal cancer cells in a simulated artificial pneumothorax model and to explore its potential mechanism of action.

METHODS

Oesophageal cancer cells were subjected to a simulated thoracoscopic CO2 pneumothorax environment with different pressures and exposure times (low-pressure group: 8 mmHg 1 h or 8 mmHg 4 h; high-pressure group: 12 mmHg 1 h). Cell viability, apoptosis, invasive capacity and mRNA expression of adhesion- and metastasis-related molecules in each group were detected. To explore in greater detail the potential reasons for the changes in biological behaviour under the high-pressure CO2 environment, we designed 3 additional experimental groups: (i) high-pressure group, (ii) hypoxia group and (iii) pH decrease group. An miRNA microarray analysis was performed by comparing 2 paired samples of cells from the high-pressure group and the control group.

RESULTS

Treatment with high-pressure CO2 pneumothorax significantly increased the cell viability (P < 0.001) and the cell invasion (P < 0.001). Significantly higher expression of adhesive- and metastasis-related molecules was also observed. Further experiments indicated that the high-pressure CO2 pneumothorax might increase cell invasion and metastasis through the high pressure and decreased pH. The miRNA microarray analysis results suggested that several potential pathways related to cancer development: the RhoA pathway, the PI3K-Akt signalling pathway and the MAPK signalling pathway.

CONCLUSIONS

The application of high-pressure CO2 pneumothorax promoted the invasion and metastasis of oesophageal cancer cells through high pressure and decreased pH. This process might be related to several signalling pathways.