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Sustained expression of miR-26a promotes chromosomal instability and tumorigenesis through regulation of CHFR.

Abstract：

:MicroRNA 26a (miR-26a) reduces cell viability in several cancers, indicating that miR-26a could be used as a therapeutic option in patients. We demonstrate that miR-26a not only inhibits G1-S cell cycle transition and promotes apoptosis, as previously described, but also regulates multiple cell cycle checkpoints. We show that sustained miR-26a over-expression in both breast cancer (BC) cell lines and mouse embryonic fibroblasts (MEFs) induces oversized cells containing either a single-large nucleus or two nuclei, indicating defects in mitosis and cytokinesis. Additionally, we demonstrate that miR-26a induces aneuploidy and centrosome defects and enhances tumorigenesis. Mechanistically, it acts by targeting G1-S transition genes as well as genes involved in mitosis and cytokinesis such as CHFR, LARP1 and YWHAE. Importantly, we show that only the re-expression of CHFR in miR-26a over-expressing cells partially rescues normal mitosis and impairs the tumorigenesis exerted by miR-26a, indicating that CHFR represents an important miR-26a target in the regulation of such phenotypes. We propose that miR-26a delivery might not be a viable therapeutic strategy due to the potential deleterious oncogenic activity of this miRNA.

journal_name

Nucleic Acids Res

journal_title

Nucleic acids research

authors

Castellano L,Dabrowska A,Pellegrino L,Ottaviani S,Cathcart P,Frampton AE,Krell J,Stebbing J

doi

10.1093/nar/gkx022

subject

Has Abstract

pub_date

2017-05-05 00:00:00

pages

4401-4412

issue

8

eissn

0305-1048

issn

1362-4962

pii

gkx022

journal_volume

45

pub_type

杂志文章

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