کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10815205 | 1058459 | 2014 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IGF-1-induced epithelial-mesenchymal transition in MCF-7 cells is mediated by MUC1
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Metastases are the major cause of death from cancer. IGF-1 signaling pathway has been shown to have strong implication in the epithelial-mesenchymal transition (EMT) process. However, the mechanisms of how IGF-1 promotes EMT have not been fully elucidated. Mucin 1 (MUC1), a transmembrane glycoprotein, engages in multiple cancer-related signaling pathways and functions as an oncoprotein that contributes to metastases. Here we provide evidence showing that IGF-1 upregulates MUC1 expression in MCF-7 cells in a PI3K/Akt signaling pathway-dependent manner. The overexpression of MUC1 is critical for IGF-1-induced EMT of MCF-7 cells because the knockdown of MUC1 prevented the EMT of MCF-7 cells as demonstrated by various EMT markers including the expression of E-cadherin, N-cadherin, vimentin, fibronectin and the nuclear translocalization of β-catenin. On the other hand, the knockdown of MUC1 had no impact on IGF-1-induced activation of PI3K/Akt or MAPK. In summary, our study demonstrated MUC1 as a critical downstream effector that mediates IGF-1-induced EMT of MCF-7 cells and suggested that MUC1 might be a potential therapeutic target for preventing tumor metastases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 26, Issue 10, October 2014, Pages 2131-2137
Journal: Cellular Signalling - Volume 26, Issue 10, October 2014, Pages 2131-2137
نویسندگان
Gaoyong Liao, Mengyu Wang, Yu Ou, Yong Zhao,