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2017 ; 40
(2
): 411-417
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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
): 411-417
PMID28627599
show 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.