Journal
CELL DEATH AND DIFFERENTIATION
Volume 17, Issue 2, Pages 246-254Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2009.117
Keywords
miR-145; ER-alpha; TP53; human BC; apoptosis; cell proliferation
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Funding
- University of Texas
- Ladjevardian Regents Research Scholar Fund
- Institutional Research Grant
- National Institutes of Health Cancer Center
- Associazione Italiana per la Ricerca sul Cancro
- Fondazione Cariplo Progetto NOBEL
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Understanding the consequences of miR-145 reintroduction in human breast cancer (BC) could reveal its tumor-suppressive functions and may disclose new aspects of BC biology. Therefore, we characterized the effects of miR-145 re-expression in BC cell lines by using proliferation and apoptosis assays. As a result, we found that miR-145 exhibited a pro-apoptotic effect, which is dependent on TP53 activation, and that TP53 activation can, in turn, stimulate miR-145 expression, thus establishing a death-promoting loop between miR-145 and TP53. We also found that miR-145 can downregulate estrogen receptor-alpha (ER-alpha) protein expression through direct interaction with two complementary sites within its coding sequence. In conclusion, we described a tumor suppression function of miR-145 in BC cell lines, and we linked miR-145 to TP53 and ER-alpha. Moreover, our findings support a view that miR-145 re-expression therapy could be mainly envisioned in the specific group of patients with ER-alpha-positive and/or TP53 wild-type tumors. Cell Death and Differentiation (2010) 17, 246-254; doi:10.1038/cdd.2009.117; published online 4 September 2009
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