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Basic Science
Fimbrial Cells Exposure to Catalytic Iron Mimics Carcinogenic Changes
  1. Debora Lattuada, PhD*,
  2. Francesca Uberti, PhD*,
  3. Barbara Colciaghi, BA*,
  4. Vera Morsanuto, MS*,
  5. Elena Maldi, MD†,
  6. Diletta Francesca Squarzanti, MS‡,
  7. Claudio Molinari, MD, PhD‡,
  8. Renzo Boldorini, MD†,
  9. Alessandro Bulfoni, MD*,
  10. Paola Colombo, MD* and
  11. Giorgio Bolis, MD*
  1. *Department of Obstetrics and Gynecology, Fondazione IRCCS Ca Granda, Ospedale Maggiore Policlinico, Milan;
  2. †Unit of Pathology, Department of Health Sciences, and
  3. ‡Physiology Laboratory, Department of Translational Medicine, University of Eastern Piedmont“Amedeo Avogadro,” Novara, Italy.
  1. Address correspondence and reprint requests to Debora Lattuada, PhD, Department of Obstetrics and Gynecology, Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico, Via Manfredo Fanti, 6, 20122 Milan, Italy. E-mail: debora.lattuada@gmail.com.

Abstract

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.

  • Fimbrial secretory epithelial cells
  • Catalytic iron
  • Epithelial ovarian cancer

http://dx.doi.org/10.1097/IGC.0000000000000379

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    Footnotes

    • Drs Debora Lattuada and Francesca Uberti contributed equally to the study and are cofirst authors.

    • The authors declare no conflicts of interest.

    • Supplemental digital content is available for this article. Direct URL citation appears in the printed text and is provided in the HTML and PDF versions of this article on the journal’s Web site (www.ijgc.net).

    • Author contribution: D.L. and F.U. conceived and designed the study. All the authors contributed to the writing of the manuscript. All the authors approved the final version of the article.