CBX7 and miR-9 are part of an autoregulatory loop controlling p16(INK) (4a).

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Title: CBX7 and miR-9 are part of an autoregulatory loop controlling p16(INK) (4a).
Author(s): O'Loghlen, A
Brookes, S
Martin, N
Rapisarda, V
Peters, G
Gil, J
Item Type: Journal Article
Abstract: Polycomb repressive complexes (PRC1 and PRC2) are epigenetic regulators that act in coordination to influence multiple cellular processes including pluripotency, differentiation, cancer and senescence. The role of PRCs in senescence can be mostly explained by their ability to repress the INK4/ARF locus. CBX7 is one of five mammalian orthologues of Drosophila Polycomb that forms part of PRC1. Despite the relevance of CBX7 for regulating senescence and pluripotency, we have a limited understanding of how the expression of CBX7 is regulated. Here we report that the miR-9 family of microRNAs (miRNAS) downregulates the expression of CBX7. In turn, CBX7 represses miR-9-1 and miR-9-2 as part of a regulatory negative feedback loop. The miR-9/CBX7 feedback loop is a regulatory module contributing to induction of the cyclin-dependent kinase inhibitor (CDKI) p16(INK4a) during senescence. The ability of the miR-9 family to regulate senescence could have implications for understanding the role of miR-9 in cancer and aging.
Publication Date: 29-Sep-2015
Date of Acceptance: 30-Aug-2015
URI: http://hdl.handle.net/10044/1/28931
DOI: https://dx.doi.org/10.1111/acel.12404
ISSN: 1474-9726
Publisher: Wiley Open Access
Start Page: 1113
End Page: 1121
Journal / Book Title: Aging Cell
Volume: 14
Issue: 6
Copyright Statement: © 2015 The Author. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Keywords: CBX7
Polycomb
miR-9
p16INK4a
senescence
CBX7
Polycomb
miR-9
p16INK4a
senescence
Developmental Biology
11 Medical And Health Sciences
06 Biological Sciences
Publication Status: Published
Appears in Collections:Clinical Sciences
Molecular Sciences
Faculty of Medicine



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