Effects of CO 2 pneumoperitoneum on proliferation, apoptosis, and migration of gastrointestinal stromal tumor cells

Abstract

Background

The purpose of the study was to investigate the proliferation and migration capability of human gastrointestinal stromal tumor line GIST-T1 after exposure to different pressures and times of CO₂ pneumoperitoneum.

Methods

We established simulated CO₂ pneumoperitoneum environment in vitro and divided the human GIST cell GIST-T1 into open control group, 8 mmHg CO₂ pneumoperitoneum treatment group and 15 mmHg CO₂ pneumoperitoneum treatment group. Each group was divided into two subgroups respectively cultured for 1 h and 3 h. pH value of cell culture, cell growth curve, and cell cycle distribution of each group was measured. By application of scratch healing tests and Transwell chamber experiments, mobility ratio and number of cells through 8 µm membranes were measured to assess the migration ability of cells in each group after intervention.

Results

Cell culture pH value of each subgroup in CO₂ group decreased significantly after exposed in CO₂ pneumoperitoneum (P < 0.01). The proliferation of GIST-T1 cells in 15 mmHg CO₂ group was significantly inhibited early (1–2 days) (P < 0.05) and the proliferation of GIST-T1 cells in 8 mmHg CO₂ 1 h subgroup and 15 mmHg CO₂ 1 h subgroup was increased significantly late (4–6 days) (P < 0.05) after the interventions of CO₂ pneumoperitoneum. The percentage of cells in G0–G1 phase increased, the percentage of S phase cells decreased (P < 0.01) in 1-h subgroup and 3-h subgroup of 15 mmHg CO₂ group 24 h after exposure to CO₂. The percentage of cells in S phase increased in 1-h subgroup of 8 mmHg CO₂ group and decreased in 3-h subgroup of 15 mmHg CO₂ group 72 h after exposure to CO₂. In the Transwell chamber experiment, the cell number through 8-µm membrane increased significantly (P < 0.01) in 3-h subgroup of CO₂ group compared to that in 3-h subgroup of control group.

Conclusions

The routine pressure and duration of CO₂ pneumoperitoneum used in clinic did not promote the proliferation of gastrointestinal stromal tumors, but had a potential risk of increasing postoperative recurrence and distant metastasis.

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