HMOX-1 inhibits TGF-β-induced epithelial-mesenchymal transition in the MCF-7 breast cancer cell line

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-beta (TGF-beta)-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-beta-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-beta-induced EMT in MCF-7 cells.