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Expression of the RAI gene is conducive to apoptosis : studies of induction and interference

Laska, Magdalena J ; Strandbygård, Dorthe ; Kjeldgaard, Anette ; Mains, Mette ; Corydon, Thomas J ; Memon, Ashfaque A LU orcid ; Sørensen, Boe S ; Vogel, Ulla ; Jensen, Uffe B and Nexø, Bjørn A (2007) In Experimental Cell Research 313(12). p.21-2611
Abstract

The RAI gene is also known as iASPP and PPP1R13L. Recent investigations have shown that the region encompassing RAI is important for the development of cancer in young and middle-aged persons. It has been speculated that the RAI product induces apoptosis by blocking NF-kappaB or inhibits apoptosis by blocking p53. Either way the gene could influence the survival of precancerous lesions. Here we report that the expression of RAI mRNA was increased in non-transformed lymphocytes and fibroblasts induced to undergo apoptosis by various means, such as treatment with etoposide, calcium ions, or interleukin-2 and/or serum deprivation. Treatment with etoposide increased the content of RAI protein, too, and caused it to translocate to the... (More)

The RAI gene is also known as iASPP and PPP1R13L. Recent investigations have shown that the region encompassing RAI is important for the development of cancer in young and middle-aged persons. It has been speculated that the RAI product induces apoptosis by blocking NF-kappaB or inhibits apoptosis by blocking p53. Either way the gene could influence the survival of precancerous lesions. Here we report that the expression of RAI mRNA was increased in non-transformed lymphocytes and fibroblasts induced to undergo apoptosis by various means, such as treatment with etoposide, calcium ions, or interleukin-2 and/or serum deprivation. Treatment with etoposide increased the content of RAI protein, too, and caused it to translocate to the nucleus. Inhibition of RAI expression in lymphocytes and fibroblasts with siRNA reduced apoptosis, but treatment with the NF-kappaB-inhibiting substance sulfasalazine relieved this dependence. In the transformed cell line HEK-293 the association between RAI induction and apoptosis seemed broken. Thus, we hypothesize that RAI induction is necessary but not sufficient for apoptosis induction in non-transformed cells. Our results could be explained by a NF-kappaB mediated mechanism.

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author
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publishing date
type
Contribution to journal
publication status
published
subject
keywords
Apoptosis/drug effects, Cell Line, Etoposide/pharmacology, Flow Cytometry, Gene Expression Regulation/drug effects, Herpes Simplex Virus Protein Vmw65/pharmacology, Humans, Intracellular Signaling Peptides and Proteins/genetics, Lymphocytes/drug effects, RNA Interference, RNA, Messenger/genetics, RNA, Small Interfering/metabolism, Repressor Proteins, Sulfasalazine/pharmacology, Time Factors, Transfection
in
Experimental Cell Research
volume
313
issue
12
pages
11 pages
publisher
Academic Press
external identifiers
  • pmid:17570360
  • scopus:34250816848
ISSN
0014-4827
DOI
10.1016/j.yexcr.2007.05.006
language
English
LU publication?
no
id
3db44eff-14f1-46e9-b8e4-7723a6560b2a
date added to LUP
2019-11-22 16:18:13
date last changed
2024-01-02 00:32:18
@article{3db44eff-14f1-46e9-b8e4-7723a6560b2a,
  abstract     = {{<p>The RAI gene is also known as iASPP and PPP1R13L. Recent investigations have shown that the region encompassing RAI is important for the development of cancer in young and middle-aged persons. It has been speculated that the RAI product induces apoptosis by blocking NF-kappaB or inhibits apoptosis by blocking p53. Either way the gene could influence the survival of precancerous lesions. Here we report that the expression of RAI mRNA was increased in non-transformed lymphocytes and fibroblasts induced to undergo apoptosis by various means, such as treatment with etoposide, calcium ions, or interleukin-2 and/or serum deprivation. Treatment with etoposide increased the content of RAI protein, too, and caused it to translocate to the nucleus. Inhibition of RAI expression in lymphocytes and fibroblasts with siRNA reduced apoptosis, but treatment with the NF-kappaB-inhibiting substance sulfasalazine relieved this dependence. In the transformed cell line HEK-293 the association between RAI induction and apoptosis seemed broken. Thus, we hypothesize that RAI induction is necessary but not sufficient for apoptosis induction in non-transformed cells. Our results could be explained by a NF-kappaB mediated mechanism.</p>}},
  author       = {{Laska, Magdalena J and Strandbygård, Dorthe and Kjeldgaard, Anette and Mains, Mette and Corydon, Thomas J and Memon, Ashfaque A and Sørensen, Boe S and Vogel, Ulla and Jensen, Uffe B and Nexø, Bjørn A}},
  issn         = {{0014-4827}},
  keywords     = {{Apoptosis/drug effects; Cell Line; Etoposide/pharmacology; Flow Cytometry; Gene Expression Regulation/drug effects; Herpes Simplex Virus Protein Vmw65/pharmacology; Humans; Intracellular Signaling Peptides and Proteins/genetics; Lymphocytes/drug effects; RNA Interference; RNA, Messenger/genetics; RNA, Small Interfering/metabolism; Repressor Proteins; Sulfasalazine/pharmacology; Time Factors; Transfection}},
  language     = {{eng}},
  month        = {{07}},
  number       = {{12}},
  pages        = {{21--2611}},
  publisher    = {{Academic Press}},
  series       = {{Experimental Cell Research}},
  title        = {{Expression of the RAI gene is conducive to apoptosis : studies of induction and interference}},
  url          = {{http://dx.doi.org/10.1016/j.yexcr.2007.05.006}},
  doi          = {{10.1016/j.yexcr.2007.05.006}},
  volume       = {{313}},
  year         = {{2007}},
}