Papers

Peer-reviewed
Jul, 2007

Heat shock proteins play a crucial role in tumor-specific apoptosis by REIC/Dkk-3

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
  • Fernando Abarzua
  • Masakiyo Sakaguchi
  • Ryuta Tanimoto
  • Hiroyuki Sonegawa
  • Dai-Wei L
  • Kohei Edamura
  • Tomoko Kobayashi
  • Masami Watanabe
  • Yuji Kashiwakura
  • Haruki Kaku
  • Takashi Saika
  • Keiichiro Nakamura
  • Yasutomo Nasu
  • Hiromi Kumon
  • Nam-Ho Huh
  • Display all

Volume
20
Number
1
First page
37
Last page
43
Language
English
Publishing type
Research paper (scientific journal)
Publisher
PROFESSOR D A SPANDIDOS

We recently showed that overexpression of REIC/Dickkopf-3 (Dkk-3), a tumor suppressor gene, induced apoptosis in a tumor cell-specific manner. The aim of the present study was to determine the mechanisms underlying the selective induction of apoptosis. At first, we found a mouse renal carcinoma cell line, RENCA, to be extremely sensitive to an adenovirus carrying REIC/Dkk-3 (Ad-REIC), and we showed that activation of c-Jun N-terminal kinase (JNK) was a critical step in cell death, i.e. a process similar to that in human prostate and testicular cancer observed in our previous studies. Among the proteins interfering with the activation of JNK, heat shock protein (Hsp)70/72 was reduced in expression in RENCA cells compared with that in NIH3T3 cells. An Hsp70/72 inducer protected RENCA cells from Ad-REIC-induced apoptosis, while an Hsp70/72 inhibitor sensitized NIH3T3 cells for apoptosis induction. These results indicate that functionally active Hsp70/72 is a key factor in tumor cell-specific induction of apoptotic cell death and that analyses of the expression levels of Hsp70/72 may be essential in determining the significance of Ad-REIC-based gene therapy against human cancer.

Link information
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000247492900005&DestApp=WOS_CPL
ID information
  • ISSN : 1107-3756
  • Web of Science ID : WOS:000247492900005

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