STAT3-decoy oligodeoxynucleotide inhibits the growth of human lung cancer via down-regulating its target genes.

Double-stranded decoy oligodeoxynucleotide (ODN) is a promising approach for inhibiting gene transcription. Signal transducer and activator of transcription (STAT) 3, a potent transcription factor, is usually constitutively activated in a variety of malignancies, and considered as an attractive drug target. In this study, it was noted that STAT3 was overactivated in human lung cancer cells, and STAT3-decoy ODN, which was high-efficiently transfected into nucleus of cancer cells, significantly inhibited the proliferation of PG cells by inducing apoptosis or cell cycle arrest. The transcription levels of mcl-1, cyclin D1, bcl-xl and survivin were significantly decreased by 64.4, 56.1, 72.8% (P<0.01) and 31.8% (P<0.05), respectively; and the synthesis levels of bcl-xl and cyclin D1 in PG cells showed 64.5% (P<0.01) and 28.6% (P<0.05) decrease, respectively. Our study demonstrated that decoy-ODN targeting at activated STAT3 may potentially be used as an anti-lung cancer therapeutic approach.