**7. Decoys**

Unlike antisense oligonucleotide approaches that target mRNA, decoys are short, doublestranded DNA molecules that compete with specific binding sites of transcription factors to prevent their binding at target promoters, in order to inhibit gene expression at pretranscrip‐ tion level. Since decoys are DNA, they are more stable and easy to handle than RNA-based intervention strategies [80]. Some methods, including the locked nucleic acid (LNA) intro‐ duced at the 3'-end [81] and chimeric decoys containing discrete binding sites [82], can increase decoys nuclease resistance and specificity. So far, numerous of studies have indicated that decoys are suited for novel potential therapeutic for combating cancer [80] and infectious diseases [83]. NOTCH1 decoy, a human IgG Fc consisting Notch1 extracellular domain inhibits tumor angiogenesis and growth by blocking Jagged-dependent activation of Notch signaling. Although well tolerated to mice for three weeks, NOTCH1 decoy treatment causes adverse severe gastrointestinal effects [84]. As above, the STAT3 (signal transducers and activators of transcription 3) decoy oligonucleotide represents another possible single-agent approach to targeting both the tumor and vascular compartments in murine tumor xenografts mediated through the inhibition of both STAT3 and STAT1 [85, 86]. Collectively, these findings point to decoys as highly attractive agents in gene-targeted therapy.
