| Literature DB >> 25490449 |
Pradeep Chaluvally-Raghavan1, Fan Zhang2, Sunila Pradeep3, Mark P Hamilton4, Xi Zhao5, Rajesha Rupaimoole6, Tyler Moss2, Yiling Lu2, Shuangxing Yu2, Chad V Pecot7, Miriam R Aure5, Sylvain Peuget8, Cristian Rodriguez-Aguayo9, Hee-Dong Han10, Dong Zhang2, Avinashnarayan Venkatanarayan11, Marit Krohn5, Vessela N Kristensen5, Mihai Gagea12, Prahlad Ram2, Wenbin Liu13, Gabriel Lopez-Berestein14, Philip L Lorenzi13, Anne-Lise Børresen-Dale5, Koei Chin15, Joe Gray15, Nelson J Dusetti8, Sean E McGuire16, Elsa R Flores11, Anil K Sood17, Gordon B Mills18.
Abstract
Small noncoding miRNAs represent underexplored targets of genomic aberrations and emerging therapeutic targets. The 3q26.2 amplicon is among the most frequent genomic aberrations in multiple cancer lineages including ovarian and breast cancers. We demonstrate that hsa-miR-569 (hereafter designated as miR569), which is overexpressed in a subset of ovarian and breast cancers, at least in part due to the 3q26.2 amplicon, alters cell survival and proliferation. Downregulation of TP53INP1 expression by miR569 is required for the effects of miR569 on survival and proliferation. Targeting miR569 sensitizes ovarian and breast cancer cells overexpressing miR569 to cisplatin by increasing cell death both in vitro and in vivo. Thus targeting miR569 could potentially benefit patients with the 3q26.2 amplicon and subsequent miR569 elevation.Entities:
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Year: 2014 PMID： 25490449 PMCID： PMC4261159 DOI： 10.1016/j.ccell.2014.10.010
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743