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Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Int+J+Mol+Med 2017 ; 40 (2): 411-7 Nephropedia Template TP
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HMOX-1 inhibits TGF-?-induced epithelial-mesenchymal transition in the MCF-7 breast cancer cell line #MMPMID28627599
Zhu X; Huang S; Zeng L; Ma J; Sun S; Zeng F; Kong F; Cheng X
Int J Mol Med 2017[Aug]; 40 (2): 411-7 PMID28627599show ga
Epithelial-mesenchymal transition (EMT) is a key mechanism underlying metastatic breast cancer. Reactive oxygen species (ROS) play an important role in EMT. Heme oxygenase-1 (HMOX-1) can reduce oxidative stress. However, the effect of HMOX-1 on the EMT process in breast cancer cells is unknown. We treated the MCF-7 breast cancer cell line with the HMOX-1 inducer hemin and observed that hemin induced HMOX-1 expression and inhibited migration, invasion and ROS generation in transforming growth factor-? (TGF-?)-treated MCF-7 cells using quantitative RT-qPCR, western blotting, wound-healing and cell invasion assays as well as fluorescent probe DCFDA. Hemin inhibited TGF-?-induced EMT in the MCF-7 cells, whereas HMOX-1 siRNA attenuated the suppressive effect of hemin as determined by the expression and cellular distribution of selected EMT markers. In summary, our results revealed that hemin treatment increased HMOX-1 expression and inhibited TGF-?-induced EMT in MCF-7 cells.