Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 37, Issue 4, Pages 1271-1278Publisher
KARGER
DOI: 10.1159/000430249
Keywords
Bone morphogenetic protein-7 (BMP7); Breast cancer; Transforming growth factor beta 1 (TGF beta 1); Epithelial-mesenchymal transition (EMT)
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Background/Aims: Bone morphogenetic protein-7 (BMP7) has been shown to reduce the severity of injury-induced fibrosis through counteracting the fibrotic effects of transforming growth factor beta 1 (TGF beta 1). However, this model in the carcinogenesis of breast cancer is unknown. Methods: We analyzed the effects of BMP7 and TGF beta 1 on gene transcripts and protein levels of EMT-related factors in breast cancer cells by RT-qPCR and Western blot, respectively. The effects of BMP7 and TGF beta 1 on cell invasiveness and migration were evaluated by scratch wound healing assay and transwell cell migration assay. The cell growth was measured by MTT assay. Results: BMP7 did not alter the TGF beta 1-stimulated phosphorylation of TGF beta receptor, but significantly inhibited the TGF beta 1-activated epithelial-mesenchymal transition (EMT)-related genes in breast cancer cells, resulting in a significant reduction in TGF beta 1-triggered cell growth and cell metastasis. Conclusion: Our data suggest that besides being a well-known antagonist for TGF beta 1 in fibrosis, BMP7 may also antagonize TGF beta 1 in tumorigenesis-associated EMT in breast cancer. Thus, BMP7 may be a promising therapeutic target for treating breast cancer. Copyright (C) 2015 S. Karger AG, Basel
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