Abstract:
:Diabetes mellitus has been related with an increased risk of breast cancer, whereas it has been suggested that links between diabetes mellitus and cancer are hyperinsulinemia, insulin resistance, hyperglycemia, and chronic inflammation induced by adipose tissue. Contribution of hyperinsulinemia to carcinogenesis is mediated through resistance to endogenous insulin and by exogenous insulin used in treatment. Epithelial to mesenchymal transition (EMT) is a process by which epithelial cells are transdifferentiated to a mesenchymal state that has been implicated in cancer progression. However, the role of insulin in EMT process has not been studied in detail. In the present study, we demonstrate that insulin induces downregulation of E-cadherin expression, accompanied with an increase of N-cadherin and vimentin expression, and an increase of MMP-2 and -9 secretions. Insulin also induces FAK activation, an increase of NFκB DNA binding activity, migration, and invasion of mammary non-tumorigenic epithelial cells MCF10A. In addition, migration requires the activity of insulin receptors and insulin-like growth factor receptor 1 (IGF1R). In summary, our results demonstrate that insulin induces an EMT-like process in MCF10A cells.
journal_name
J Cell Biochemjournal_title
Journal of cellular biochemistryauthors
Rodriguez-Monterrosas C,Díaz-Aragon R,Leal-Orta E,Cortes-Reynosa P,Perez Salazar Edoi
10.1002/jcb.26582subject
Has Abstractpub_date
2018-05-01 00:00:00pages
4061-4071issue
5eissn
0730-2312issn
1097-4644journal_volume
119pub_type
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