Decoy receptor 3 (DcR3) is a supermember of tumor necrosis receptor (TNF) factor. DcR3
acts as a binding partner in multiple apoptotic ligands that inhibit apoptosis. DcR3 has been
shown to sensitize cells to TNF-associated apoptosis-inducing ligand (TRAIL)-induced
apoptosis. DcR3 has been shown to be a 'pleiotropic' effective soluble factor to modulate cell
functions by its 'decoy' and 'non-decoy' actions. Recombinant DcR3 fused with an IgG1 Fc
domain can inhibit the interaction between Fas and FasL. TNF superfamily FasL can inhibit
apoptosis and increase angiogenesis through neutralizing members of LIGHT and TL1A.
DcR3 serum level is almost undetectable in most normal individuals without inflammatory
diseases and cancer. There are studies showing that serum DcR3 level is also associated with
cancer staging in cancer patients. High DcR3 levels in serum or tissues have been found to be
associated with poor prognosis and/or resistance to therapy in some cancer patients.
Therefore, in the future it will be possible to predict the outcome of disease severity by
determining the cut-off value of the DcR3 serum level.
While inhibition of DcR3 expression may attenuate tumor growth, enhancement of DcR3-
mediated effector functions may be a promising approach to attenuate autoimmunity and
promote tissue repair. Thus, recombinant DcR3 is a promising therapeutic agent for
immunotherapy, however, turning off DcR3 expression in the cancerous setting may increase
the efficacy of cancer therapy.
The purpose of this review is to provide clinical convenience by collecting the findings of
studies on DcR3 so far.
These findings may be useful for diagnosis, differentiation, metastasis and detection of cancer
stages. Furthermore, these may provide new therapeutic approaches to target carcinomas in
the future.
Key words: DcR3; DcR3 and cancer; Biomarker
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