Interleukin-6 induces epithelial-mesenchymal transition in breast cancer cells

Abstract

Background: Breast cancer is the leading cause of cancer-related death in Mexico, with most deaths being related to locally advanced or metastatic disease at diagnosis. Epithelial-mesenchymal transition (EMT) is one of the steps that are indispensable for metastasis. Different factors trigger EMT, like TGF-β, EGF and interleukin 6 (IL-6), among others. EMT is characterized by E-cadherin expression loss and N-cadherin and vimentin expression. In this study, we investigated the role of IL-6 on EMT induction. Methods: MBCDF and MBCD17 primary breast cancer cell cultures were used. E-cadherin expression was measured by Western Blot. Cells were stimulated with IL-6 to induce EMT. STAT3 activation was measured using phospho-specific antibodies, and E-cadherin expression was measured as EMT marker. Results: MBCDF and MBCD17 primary breast cancer cell cultures stimulation with IL-6 induced STAT3-Tyr705 phosphorylation without its total levels being altered; in addition, IL-6 cell-stimulation was shown to induce EMT, as evidenced by E-cadherin loss. Conclusions:The results of the present work suggest that IL-6 induces EMT in primary breast cancer cell cultures through STAT3 phosphorylation. (creativecommons.org/licenses/by-nc-nd/4.0/).