期刊
ONCOTARGET
卷 8, 期 62, 页码 104855-104866出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.20418
关键词
doxycycline; miR-17; EMT; GPCR; NF-kappa B
资金
- National Natural Science Funds of China [81572838, 81402973]
- Key Technologies RAMP
- D Program of Tianjin [11ZCKFSY06900]
- Tianjin Natural Science and Technology Fund [15JCYBJC26400]
- Foundation for the Author of National Excellent Doctoral Dissertation of China [201482]
Doxycycline displays high efficiency for cancer therapy. However, the molecular mechanism is poorly understood. In our previous study, doxycycline was found to suppress tumor progression by directly targeting proteinase-activated receptor 1 (PAR1). In this study, microRNAs were found to be involved in PAR1-mediated antitumor effects of doxycycline. Among these miRNAs, miR-17 was found to promote breast cancer cell metastasis both in vivo and in vitro. Moreover, miR-17 could reverse partial doxycycline inhibition effects on breast cancer. Employing luciferase and chromatin immunoprecipitation assays, nuclear factor-kappaB (NF-kappa B) was found to bind miR-17 promoters. Furthermore, E-cadherin was identified as the target gene of miR-17. These results showed that miR-17 can resist the inhibitory effects of doxycycline on breast cancer epithelial-mesenchymal transformation (EMT) by targeting E-cadherin.
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