Breast implants are widely used and at times might cause inflammation as a foreign body, followed by fibrous capsule formation around the implant. In cancer, the inflamed stroma is essential for preservation of the tumor. Mesenchymal stem cells can be recruited to sites of inflammation, and their role in cancer development is debated. The authors assessed the effects of inflammation caused by breast implants’ effects on tumor.
Mesenchymal stem cells were isolated from the fibrous capsules of women who underwent a second operation after 1 year (presenting inflammation) or after 20 years (not presenting inflammation) since initial surgery. After characterization, cells were co-cultured with MCF7, a breast cancer cell line. The expression of genes involved in oncogenesis, proliferation, and epithelial-to-mesenchymal transition was investigated, followed by Western blot analyses.
After co-culture with mesenchymal stem cells from the inflamed capsule, MCF7 induced a dose- and time-dependent increase in proliferation. Polymerase chain reaction analyses revealed a dysregulation of genes involved in oncogenesis, proliferation, and epithelial-to-mesenchymal transition. The subsequent evaluation by Western blot did not confirm these results, showing only a modest decrease in the expression of E-cadherin after co-culture with mesenchymal stem cells (both derived from inflamed or control capsules).
These data indicate that inflammation caused by breast implants partially affects proliferation of MCF7 but does not influence key mechanisms of tumor development.
From the Departments of Clinical and Molecular Sciences–Histology and Experimental and Clinical Medicine–Clinic of Plastic and Reconstructive Surgery, Università Politecnica delle Marche; and the Clinic of Medical Oncology, AO Ospedali Riuniti-Università Politecnica delle Marche.
The first two authors contributed equally to the work.
Disclosure: None of the authors has a financial interest in any of the products or devices mentioned in this article.
Received for publication March 12, 2013; accepted July 1, 2013.
Monia Orciani, Ph.D., Department of Clinical and Molecular Sciences–Histology, Università Politecnica delle Marche, Via Tronto 10/A 60020, Ancona, Italy, email@example.com