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‑β (TGF‑β)‑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‑β‑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‑β‑induced EMT in MCF‑7 cells.