Linked Life Data

20705054

Source:http://linkedlifedata.com/resource/pubmed/id/20705054

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-9-13
pubmed:abstractText
Smooth muscle protein 22-alpha (SM22?) is known as a transformation- and shape change-sensitive actin cross-linking protein found in smooth muscle tissue and fibroblasts; however, its functional role remains uncertain. We reported previously that SM22? overexpression confers resistance against anti-cancer drugs or radiation via induction of metallothionein (MT) isozymes in HepG2 cells. In this study, we demonstrate that SM22? overexpression leads cells to a growth arrest state and promotes cellular senescence caused by treatment with a subclinical dose of ?-radiation (0.05 and 0.1 Gy) or doxorubicin (0.01 and 0.05 ?g/ml), compared to control cells. Senescence growth arrest is known to be controlled by p53 phosphorylation/p21(WAF1/Cip1) induction or p16(INK4a)/retinoblastoma protein (pRB) activation. SM22? overexpression in HepG2 cells elevated p16(INK4a) followed by pRB activation, but did not activate the p53/p21(WAF1/Cip1) pathway. Moreover, MT-1G, which is induced by SM22? overexpression, was involved in the activation of the p16(INK4a)/pRB pathway, which led to a growth arrest state and promoted cellular senescence caused by damaging agents. Our findings provide the first demonstration that SM22? modulates cellular senescence caused by damaging agents via regulation of the p16(INK4a)/pRB pathway in HepG2 cells and that these effects of SM22? are partially mediated by MT-1G.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1090-2104
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
400
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
100-5
pubmed:dateRevised
2011-11-10
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
SM22?-induced activation of p16INK4a/retinoblastoma pathway promotes cellular senescence caused by a subclinical dose of ?-radiation and doxorubicin in HepG2 cells.
pubmed:affiliation
Department of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute, Daejeon, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't