Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells
Stem cells aging: balancing self-renewal halt with complexity Mounting evidence suggests a link between cellular senescence and human adult stem cell function upon aging. Senescence is often viewed as an intrinsic program to prevent oncogenic transformation. However, the collaborative research lead...
Guardado en:
Autores principales: | , , , , , , , , , , , |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Nature Portfolio
2017
|
Materias: | |
Acceso en línea: | https://doaj.org/article/e3010ed26bd14b8ca45b854bb7cfd1b4 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
id |
oai:doaj.org-article:e3010ed26bd14b8ca45b854bb7cfd1b4 |
---|---|
record_format |
dspace |
spelling |
oai:doaj.org-article:e3010ed26bd14b8ca45b854bb7cfd1b42021-12-02T14:22:33ZOpposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells10.1038/s41514-017-0006-y2056-3973https://doaj.org/article/e3010ed26bd14b8ca45b854bb7cfd1b42017-04-01T00:00:00Zhttps://doi.org/10.1038/s41514-017-0006-yhttps://doaj.org/toc/2056-3973Stem cells aging: balancing self-renewal halt with complexity Mounting evidence suggests a link between cellular senescence and human adult stem cell function upon aging. Senescence is often viewed as an intrinsic program to prevent oncogenic transformation. However, the collaborative research lead by Aelan Cell Technologies suggests that replicative senescence might be more dynamic than previously anticipated. Integrated genomic and proteomic analyses of human adult stem cells revealed that subset of senescence-associated miRNAs (SA-miRNA) functionally required for establishing senescence, act to provide an intricate balance between driving and restraining cancerous events upon senescence. It is commonly believed that cancer arises as a consequence of an imbalance in cellular homeostasis. These new results shed light on the fundamental role of these SA-miRNA as functionally antagonistic regulators of gene networks, future exploration of which can help us understand the etiology underlying age-related disease and cancer.Mary F. LopezPing NiuLu WangMaryann VogelsangMeenakshi GaurBryan KrastinsYueqiang ZhaoAibek SmagulAliya NussupbekovaAikan A. AkanovI. King JordanVictoria V. LunyakNature PortfolioarticleGeriatricsRC952-954.6ENnpj Aging and Mechanisms of Disease, Vol 3, Iss 1, Pp 1-15 (2017) |
institution |
DOAJ |
collection |
DOAJ |
language |
EN |
topic |
Geriatrics RC952-954.6 |
spellingShingle |
Geriatrics RC952-954.6 Mary F. Lopez Ping Niu Lu Wang Maryann Vogelsang Meenakshi Gaur Bryan Krastins Yueqiang Zhao Aibek Smagul Aliya Nussupbekova Aikan A. Akanov I. King Jordan Victoria V. Lunyak Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells |
description |
Stem cells aging: balancing self-renewal halt with complexity Mounting evidence suggests a link between cellular senescence and human adult stem cell function upon aging. Senescence is often viewed as an intrinsic program to prevent oncogenic transformation. However, the collaborative research lead by Aelan Cell Technologies suggests that replicative senescence might be more dynamic than previously anticipated. Integrated genomic and proteomic analyses of human adult stem cells revealed that subset of senescence-associated miRNAs (SA-miRNA) functionally required for establishing senescence, act to provide an intricate balance between driving and restraining cancerous events upon senescence. It is commonly believed that cancer arises as a consequence of an imbalance in cellular homeostasis. These new results shed light on the fundamental role of these SA-miRNA as functionally antagonistic regulators of gene networks, future exploration of which can help us understand the etiology underlying age-related disease and cancer. |
format |
article |
author |
Mary F. Lopez Ping Niu Lu Wang Maryann Vogelsang Meenakshi Gaur Bryan Krastins Yueqiang Zhao Aibek Smagul Aliya Nussupbekova Aikan A. Akanov I. King Jordan Victoria V. Lunyak |
author_facet |
Mary F. Lopez Ping Niu Lu Wang Maryann Vogelsang Meenakshi Gaur Bryan Krastins Yueqiang Zhao Aibek Smagul Aliya Nussupbekova Aikan A. Akanov I. King Jordan Victoria V. Lunyak |
author_sort |
Mary F. Lopez |
title |
Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells |
title_short |
Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells |
title_full |
Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells |
title_fullStr |
Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells |
title_full_unstemmed |
Opposing activities of oncogenic MIR17HG and tumor suppressive MIR100HG clusters and their gene targets regulate replicative senescence in human adult stem cells |
title_sort |
opposing activities of oncogenic mir17hg and tumor suppressive mir100hg clusters and their gene targets regulate replicative senescence in human adult stem cells |
publisher |
Nature Portfolio |
publishDate |
2017 |
url |
https://doaj.org/article/e3010ed26bd14b8ca45b854bb7cfd1b4 |
work_keys_str_mv |
AT maryflopez opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT pingniu opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT luwang opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT maryannvogelsang opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT meenakshigaur opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT bryankrastins opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT yueqiangzhao opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT aibeksmagul opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT aliyanussupbekova opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT aikanaakanov opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT ikingjordan opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells AT victoriavlunyak opposingactivitiesofoncogenicmir17hgandtumorsuppressivemir100hgclustersandtheirgenetargetsregulatereplicativesenescenceinhumanadultstemcells |
_version_ |
1718391521420509184 |