PT - JOURNAL ARTICLE AU - Debora Lattuada AU - Francesca Uberti AU - Barbara Colciaghi AU - Vera Morsanuto AU - Elena Maldi AU - Diletta Francesca Squarzanti AU - Claudio Molinari AU - Renzo Boldorini AU - Alessandro Bulfoni AU - Paola Colombo AU - Giorgio Bolis TI - Fimbrial Cells Exposure to Catalytic Iron Mimics Carcinogenic Changes AID - 10.1097/IGC.0000000000000379 DP - 2015 Mar 01 TA - International Journal of Gynecologic Cancer PG - 389--398 VI - 25 IP - 3 4099 - http://ijgc.bmj.com/content/25/3/389.short 4100 - http://ijgc.bmj.com/content/25/3/389.full SO - Int J Gynecol Cancer2015 Mar 01; 25 AB - Objective Recent evidence strongly suggests that the fallopian tube is a site of origin of ovarian cancer. Although histological data show iron deposition in the fallopian tubes, its role remains unclear. To establish whether catalytic iron has a possible role in ovarian carcinogenesis, we isolated human fimbrial secretory epithelial cells (FSECs).Methods Fimbrial secretory epithelial cells, isolated from women undergoing isteroannessiectomy, were treated with different doses of catalytic iron (0.05–100 mM) to study cell viability; NO production; p53, Ras, ERK/MAPK, PI3K/Akt, Ki67, and c-Myc protein expressions through Western blot analysis; and immunocytochemistry or immunofluorescence.Results In FSECs treated with catalytic iron for up to 6 days, we observed an increase in cell viability, NO production, and p53, pan-Ras, ERK/MAPK, PI3K/Akt, Ki67, and c-Myc activations (P < 0.05) in a dose-dependent and time-dependent manner. These same results were also observed in FSECs maintained for respectively 2 and 4 weeks in the absence of catalytic iron after 6 days of stimulation.Conclusions Our model aimed at studying the main nongenetic risk factor for ovarian cancer, providing an alternative interpretation for the role of menstruation in increasing risk of this pathology. This in vitro model mimics several features of the precursor lesions and opens new scenarios for further investigations regarding the correlation between damages produced by repeated retrograde menstruation carcinogenic stimuli.