Jul 8, 2020

NR2F2 plays a major role in insulin-induced epithelial-mesenchymal transition in breast cancer cells

BMC Cancer
Baili XiaYi Ding

Abstract

The failure of treatment for breast cancer usually results from distant metastasis in which the epithelial-mesenchymal transition (EMT) plays a critical role. Hyperinsulinemia, the hallmark of Type 2 diabetes mellitus (T2DM), has been regarded as a key risk factor for the progression of breast cancer. Nuclear receptor subfamily 2, group F, member 2 (NR2F2) has been implicated in the development of breast cancer, however its contribution to insulin-induced EMT in breast cancer remains unclear. Overexpression and knockdown of NR2F2 were used in two breast cancer cell lines, MCF-7 and MDA-MB-231 to investigate potential mechanisms by which NR2F2 leads to insulin-mediated EMT. To elucidate the effects of insulin and signaling events following NR2F2 overexpression and knockdown, Cells' invasion and migration capacity and changes of NR2F2, E-cadherin, N-cadherin and vimentin were investigated by real-time RT-PCR and western blot. Insulin stimulation of these cells increased NR2F2 expression levels and promoted cell invasion and migration accompanied by alterations in EMT-related molecular markers. Overexpression of NR2F2 and NR2F2 knockdown demonstrated that NR2F2 expression was positively correlated with cell invasion, migration and...Continue Reading

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Mentioned in this Paper

Malignant Neoplasm of Breast
Migration, Cell
Steroid hormone receptor
Breast Cancer Cell
Gene Knockdown Techniques
E-Cadherin
ApoAI regulatory protein-1
CDH1
Epithelial to Mesenchymal Transition
CDH2

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