Article Text
PDF
Abstract
Introduction Endometrial cancer is a growing health concern for women worldwide. Endometrial cancer is associated with several risk but less considering microbiota in cancer mechanism. Our published work indicates Porphyromas somerae is associated with endometrial cancer and invade endometrial cancer cells. Our transcriptomic data indicates elevated C3 expression in benign host after exposing to P.somerae. Our hypothesis is that exposure of benign menstrual stem cells to P. somerae promotes a rise in complement system (C3) translation.
Methods Menstrual stem cells and endometrial cancer cell line (KLE) were inoculated and incubated with P.somerae under hypoxic conditions (5% O2) for 4 h.Cell culture supernatant and host cells were collected at 0,4, 24,48,72 and 168 hours. Three replicates per experimental arm were used. Cell lysate and culture supernatant C3 concentrations were measured in duplicate through Enzyme-linked Immunosorbent Assays via manufacture protocols. T-test was used for statistics and P<0.05 was recognized as statistical significance.
Results Cell culture supernatant and host cell’s C3 protein level was higher in supernatant than host cells for both cell lines.(figure 1,2) C3 level was higher in MSC exposed to P.somerae than unexposed MSC. KLE C3 protein levels were higher than MSC, but exposure to P.somerae did not significantly alter C3 levels in the KLE cell line.
Conclusion/Implications Our results indicate MSC exposing to P. somerae has higher C3 concentrations. We verified KLE cells have higher C3 concentration than MSC, as literature C3 elevated in endometrial cancer. Future work will explore the impact of other microbiome on C3 levels and downstream effects of endometrial cancer pathogenesis.
