Higher CO2-insufflation pressure inhibits the expression of adhesion molecules and the invasion potential of colon cancer cells.

AIM: To investigate the influence of CO(2)-insufflation pressure on adhesion, invasion and metastatic potential of colon cancer cells based on adhesion molecules expression.
METHODS: With an in vitro artificial pneumoperitoneum model, SW1116 human colon carcinoma cells were exposed to CO(2)-insufflation in 5 different pressure groups: 6 mmHg, 9 mmHg, 12 mmHg, 15 mmHg and control group, respectively for 1 h. Expression of E-cadherin, ICAM-1, CD44 and E-selectin was measured at 0, 12, 24, 48 and 72 h after CO(2)-insufflation using flow cytometry. The adhesion and invasion capacity of SW1116 cells before and after exposure to CO(2)-insufflation was detected by cell adhesion/invasion assay in vitro. Each group of cells was injected intraperitoneally into 16 BALB/C mice. The number of visible abdominal cavity tumor nodules, visceral metastases and survival of the mice were recorded in each group.
RESULTS: The expression of E-cadherin, ICAM-1, CD44 and E-selectin in SW1116 cells were changed significantly following exposure to CO(2) insufflation at different pressures (P < 0.05). The expression of E-cadherin, CD44 and ICAM-1 decreased with increasing CO(2)-insufflation pressure. The adhesive/invasive cells also decreased gradually with increasing pressure as determined by the adhesion/invasion assay. In animal experiments, the number of abdominal cavity tumor nodules in the 15 mmHg group was also significantly lower than that in the 6 mmHg group (29.7 +/- 9.91 vs 41.7 +/- 14.90, P = 0.046). However, the survival in each group was not statistically different.
CONCLUSION: CO(2)-insufflation induced a temporary change in the adhesion and invasion capacity of cancer cells in vitro. Higher CO(2)-insufflation pressure inhibited adhesion, invasion and metastatic potential in vitro and in vivo, which was associated with reduced expression of adhesion molecules.