Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells.



Lopez, Mary F, Niu, Ping, Wang, Lu, Vogelsang, Maryann, Gaur, Meenakshi, Krastins, Bryan, Zhao, Yueqiang, Smagul, Aibek, Nussupbekova, Aliya, Akanov, Aikan A
et al (show 2 more authors) (2017) Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells. NPJ aging and mechanisms of disease, 3. 7 - ?.

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Abstract

Growing evidence suggests that many diseases of aging, including diseases associated with robust changes and adipose deports, may be caused by resident adult stem cell exhaustion due to the process called cellular senescence. Understanding how microRNA pathways can regulate cellular senescence is crucial for the development of novel diagnostic and therapeutic strategies to combat these pathologies. Herein, using integrated transcriptomic and semi-quantitative proteomic analysis, we provide a system level view of the regulation of human adipose-derived stem cell senescence by a subset of mature microRNAs (termed senescence-associated-microRNAs) produced by biogenesis of oncogenic <i>MIR17HG</i> and tumor-suppressive <i>MIR100HG</i> clusters. We demonstrate functional significance of these mature senescence-associated-microRNAs in the process of replicative senescence of human adipose-derived stem cells ex-vivo and define a set of senescence-associated-microRNA gene targets that are able to elicit, modulate and, most importantly, balance intimate connections between oncogenic and senescent events.

Item Type: Article
Depositing User: Symplectic Admin
Date Deposited: 31 May 2019 10:06
Last Modified: 07 Oct 2021 07:11
DOI: 10.1038/s41514-017-0006-y
Open Access URL: https://doi.org/10.1038/s41514-017-0006-y
URI: https://livrepository.liverpool.ac.uk/id/eprint/3043818