T136: An oxidative stress during laproscopic surgery is a possible triggering factor of cancer cell metastasis

Abstract

Objective To study the impact of oxidative stress acute hypoxia and reperfusion on HeLa cervical cancer cell attachment, survival and invasion capacities. Summary background data Many hypotheses have been proposed to explain the mechanism of port-site metastases (PSM). We presumed that CO2 exposure results in hypoxia and reperfusion with subsequent oxidative stress of cancer cells being a triggering mechanism of PSM. Methods Two CO2-pneumoperitoneum conditions were created: the hypoxic standard model (HSM) and oxidative stress model (OSM) upon CO2 insufflation and reperfusion by means of in vitro cell culture tools and non-exposed cells were served as intact control. HeLa cervical cancer cells were exposed under these CO2 insufflation conditions. Subsequently, HeLa cell attachment, viability and proliferation capacities were evaluated in duplicate samples as series I and II by the MTT and SRB assays and invasion by the Matrigel invasion assay and repeated in triplicate experiments. The impact of different CO2-pneumoperitoneum conditions on cancer cell attachment was evaluated immediately after exposure, whereas invasion capacity after 48 h of incubation and survival and proliferation every 24 h for 72 h. Results Both CO2 insufflation models significantly affected HeLa cell attachment activity ( p p p p p Conclusion An in vitro model of oxidative stress during CO2-pneumoperitoneum increased HeLa cancer cell invasion capacity in comparison with standard CO2-pneumoperitoneum condition with continuous CO2 insufflation. Oxidative stress followed by acute hypoxia and reperfusions during deflations can increase cancer cell attachment and survival capacity, and may trigger cancer cell invasion and metastasis. These data suggest that a regime of laparoscopic procedures may affect attachment and invasion of cancer cells and hence can explain the occurrence of port-site cancer metastasis.