Insulin induces an EMT-like process in mammary epithelial cells MCF10A.

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 Biochem

authors

Rodriguez-Monterrosas C,Díaz-Aragon R,Leal-Orta E,Cortes-Reynosa P,Perez Salazar E

doi

10.1002/jcb.26582

subject

Has Abstract

pub_date

2018-05-01 00:00:00

pages

4061-4071

issue

5

eissn

0730-2312

issn

1097-4644

journal_volume

119

pub_type

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