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- Title
Estradiol, TGF-β1 and hypoxia promote breast cancer stemness and EMT-mediated breast cancer migration.
- Authors
SEONG-JOON PARK; JOONG-GOOK KIM; NAM DEUK KIM; KWANGMO YANG; JAE WOONG SHIM; KYU HEO
- Abstract
Breast cancer is one of the most common cancer types among women, acting as a distinct cause of mortality, and has a high incidence of recurrence. External stimuli, including 17β-estradiol (E2), transforming growth factor (TGF)-β1 and hypoxia, may be important in breast cancer growth and metastasis. However, the effects of these stimuli on breast cancer stem cell (CSC) regulation have not been fully investigated. In the present study, the proportion of cluster of differentiation (CD)44+/CD24-/low cells increased following treatment with E2, TGF-β1 and hypoxia in MCF-7 cells. The expression of CSC markers, including SOX2, KLF4 and ABCG2, was upregulated continually by E2, TGF-β1 and hypoxia. In addition, the expression levels of epithelial-mesenchymal transition-associated factors increased following treatment with E2, TGF-β1 and hypoxia. Therefore, the migration ability of E2-, TGF-β1- and hypoxia-treated MCF-7 cells was enhanced compared with control cells. In addition, the enhancement of apoptosis by 5-flurouracil or radiation was abolished following treatment with E2, TGF-β1 and hypoxia. These results indicate that E2, TGF-β1 and hypoxia are important for regulating breast CSCs, and that the modulation of the microenvironment in tumors may improve the efficiency of breast cancer therapy.
- Subjects
GENETICS of breast cancer; PHYSIOLOGICAL effects of estradiol; TRANSFORMING growth factors-beta; HYPOXEMIA; CELL migration; MESENCHYMAL stem cells; CELL transformation; SOX transcription factors
- Publication
Oncology Letters, 2016, Vol 11, Issue 3, p1895
- ISSN
1792-1074
- Publication type
Article
- DOI
10.3892/ol.2016.4115