Thioredoxin overexpression in HT-1080 cells induced cellular senescence and sensitization to gamma radiation

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Title
Thioredoxin overexpression in HT-1080 cells induced cellular senescence and sensitization to gamma radiation
Author(s)
H S Byun; Eun Wie Cho; J S Kim; M S Moon; J J Yum; K C Kim; I G Kim
Bibliographic Citation
FEBS Letters, vol. 579, no. 19, pp. 4055-4062
Publication Year
2005
Abstract
An increment of thioredoxin-1 (TRX) is observed in many human primary cancers and appears to contribute to an increase of cell growth and a resistance to chemotherapy. On the contrary, when TRX was overexpressed in the HT-1080 fibrosarcoma cells, the cell growth was retarded and chromosomal polyploidy and cellular senescence were induced. TRX-overexpression made HT-1080 cells resistant to an oxidative stress caused by H2O2 or paraquat. But these cells were significantly sensitive to ionizing radiation, showing an abrogation of the G2 checkpoint. Their DNA contents were twice of the controls and they expressed typical senescence markers. Their expression levels of p53 and cyclin-dependent kinase inhibitors (CDKI) were about 2-3-fold higher than the control. Nevertheless, cyclin D1 and D3, which are negatively regulated by CDKIs, were also increased. Overall, in HT-1080 cells the TRX-overexpression created a state of cellular senescence caused by a simultaneous stimulation of the mitogen-activated pathways and an inhibition of the cyclin-dependent kinases, which is known as a hypermitogenic arrest.
Keyword
cellular senescencecyclin D1HT-1080polyploidythioredoxin
ISSN
0014-5793
Publisher
Wiley
DOI
http://dx.doi.org/10.1016/j.febslet.2005.06.023
Type
Article
Appears in Collections:
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
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