| Literature DB >> 22911661 |
Elizabeth C Martin1, Steven Elliott, Lyndsay V Rhodes, James W Antoon, Claire Fewell, Yun Zhu, Jennifer L Driver, Mona Jodari-Karimi, Christopher W Taylor, Erik K Flemington, Barbara S Beckman, Bridgette M Collins-Burow, Matthew E Burow.
Abstract
microRNAs (miRNA) are regulators of cellular pathways and alterations of normal miRNA expression levels have been shown to increase tumorigenesis. miR-24 has been demonstrated as having both tumor suppressive and oncogenic properties depending on cell context. Here, we demonstrate a possible role for pre-miR-24-2 as a tumor suppressor in the MCF-7 breast cancer cell line through the preferential processing of mature miR-24-2* over miR-24. Specifically, we show that the ectopic expression of miR-24-2* in MCF-7 breast cancer cells results in a suppression of cellular survival both in vivo and in vitro. Notably, the overexpression of miR-24-2* results in a dampening of cell survival through the targeted suppression of PKCα. In addition, a similar biological change is observed in vivo where MCF-7 cells overexpressing pre-miR-24-2 have decreased tumorigenicity and tumor incidence. Taken together our data demonstrate that when overexpressed biogenesis of the pre-miR-24-2 favors miR-24-2* in the MCF-7 breast cancer cell line and suggests a tumor suppressive role for miR-24-2* observed through the inhibition of PKCα-mediated cellular survival.Entities:
Keywords: PKCα cellular survival; breast cancer; miR-24-2*; miRNA maturation; strand preference
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Year: 2012 PMID: 22911661 PMCID: PMC4030540 DOI: 10.1002/mc.21946
Source DB: PubMed Journal: Mol Carcinog ISSN: 0899-1987 Impact factor: 4.784