Journal
CANCER LETTERS
Volume 323, Issue 2, Pages 171-179Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2012.04.010
Keywords
Angiogenin; MicroRNA; Vascularization; Tumorigenesis; Metastasis
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Funding
- National High-tech R&D Program of China (863 Program [2008AA02Z101]
- National Natural Science Foundation of China [30770470]
- Zhejiang Provincial Natural Science Foundation of China [Z206034]
- Zhejiang Provincial Program for the Cultivation of High-level Innovative Health Talents
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Although the expression of angiogenin (ANG), an angiogenic and tumorigenic factor, is elevated in various types of cancers, its regulation mechanism remains unclear. In the present study, in silica search predicted that miR-409-3p targeted to the 3' untranslated region (3'UTR) of the ANG mRNA. Overexpression of miR-409-3p in fibrosarcoma HT1080 cells resulted in decreased steady-state level of ANG transcript and ANG production which were achieved through direct binding of this miRNA to the ANG 3'UTR. The suppressions of miR-409-3p to rRNA transcription, cell proliferation and vasculogenic mimicry could be partially restored by overexpression of ANG with a mutated binding site of miR-409-3p within the ANG 3'UTR. Ectopic expression of miR-409-3p in transplanted HT1080 cells led to the retardation of tumor growth, vascularization and lung metastasis in mouse tumor xenografts. In these xenografts tissues, the expression of miR-409-3p displayed an inverse correlation with ANG, which was also detected in human fibrosarcoma samples. In addition, the suppression effects of miR-409-3p on cell proliferation and angiogenesis in vitro were also found in human umbilical vein endothelial cells. Taken together, these data demonstrate that miR-409-3p inhibits tumor growth, vascularization and metastasis through down-regulating ANG expression. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
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