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RESEARCH PAPER
WISP-1 attenuates p53-mediated apoptosis in response to DNA damage through activation of the Akt kinase
Fei
Su,
Michael
Overholtzer,
Daniel
Besser, and
Arnold J.
Levine1
Laboratory of Cancer Biology, The Rockefeller University,
New York, New York 10021-6399, USA
WISP-1 (Wnt-1-induced
secreted protein) was identified as an oncogene
regulated by the Wnt-1--catenin pathway. WISP-1 belongsto the CCN
family of growth factors, which are cysteine-rich,heparin-binding,
secreted proteins associated with the extracellularmatrix, and can
interact with cellular integrins. Expression ofWISP-1 in
some cells results in transformation and tumorigenesis.Here it is
shown that WISP-1 can activate the antiapoptotic Akt/PKBsignaling
pathway. It also is demonstrated that WISP-1 can preventcells from
undergoing apoptosis following DNA damage through inhibitionof the
mitochondrial release of cytochrome c and up-regulationof
antiapoptotic Bcl-XL. Furthermore, the results show that
WISP-1protects cells from p53-dependent cell death, but not Fas-ligandactivated cell death, suggesting that there may be cross talkbetween
the tumor suppressor protein p53 and WISP-1 signalingpathways. WISP-1 acts to
block cell death at a late stage in thep53-mediated apoptosis pathway.
[Key Words:
WISP-1; Akt; apoptosis; p53; DNA damage]
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|Abstract »|Full Text »|PDF »
-catenin pathway. WISP-1 belongs to the CCN
family of growth factors, which are cysteine-rich, heparin-binding,
secreted proteins associated with the extracellular matrix, and can
interact with cellular integrins. Expression of WISP-1 in
some cells results in transformation and tumorigenesis. Here it is
shown that WISP-1 can activate the antiapoptotic Akt/PKB signaling
pathway. It also is demonstrated that WISP-1 can prevent cells from
undergoing apoptosis following DNA damage through inhibition of the
mitochondrial release of cytochrome c and up-regulation of
antiapoptotic Bcl-XL. Furthermore, the results show that
WISP-1 protects cells from p53-dependent cell death, but not Fas-ligand activated cell death, suggesting that there may be cross talk between
the tumor suppressor protein p53 and WISP-1 signaling pathways. WISP-1 acts to
block cell death at a late stage in the p53-mediated apoptosis pathway.
