Objective: The effect of CO2 pneumoperitoneum (CDP) on the oncology outcomes of patients undergoing laparoscopic radical hysterectomy for cervical cancer remains unclear. In this study, we investigated the effects of CDP on the proliferation of cervical cancer cells and examined the molecular mechanism.
Materials and methods: We established an in vitro CDP model to study the effects of CDP on the proliferation of cervical cancer cells by Cell Counting Kit-8 (CCK-8) assay, xenografted tumor assay. Tandem mass tag-based quantitative proteomics were used to study the proteomic changes in HeLa cells after CDP treatment. Western blot assay was used to detect the expressions of PI3K/Akt signaling pathway proteins.
Results: CDP increased cell proliferation after a short period of inhibition in vitro and promoted tumorigenesis in vivo. Proteomic analysis showed that the expression levels of 177 and 309 proteins were changed significantly 24 and 48 h after CDP treatment, respectively. The acidification caused by CO2 inhibited the proliferation of cervical cancer cells by inhibiting the phosphorylation of PI3K and Akt.
Conclusions: CDP promoted the proliferation of human cervical cancer cells after a short time of inhibition. The mechanism of which is related to the inhibition of phosphorylation of the PI3K/Akt signaling pathway.
Keywords: CO2 pneumoperitoneum; Cervical cancer; PI3K/Akt Signaling pathway; laparoscopy; proteomics.