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© Research
Publication : BMC cell biology

A STAT3-decoy oligonucleotide induces cell death in a human colorectal carcinoma cell line by blocking nuclear transfer of STAT3 and STAT3-bound NF-κB

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in BMC cell biology - 12 Apr 2011

Souissi I, Najjar I, Ah-Koon L, Schischmanoff PO, Lesage D, Le Coquil S, Roger C, Dusanter-Fourt I, Varin-Blank N, Cao A, Metelev V, Baran-Marszak F, Fagard R

Link to Pubmed [PMID] – 21486470

BMC Cell Biol. 2011 Apr;12:14

The transcription factor STAT3 (signal transducer and activator of transcription 3) is frequently activated in tumor cells. Activated STAT3 forms homodimers, or heterodimers with other TFs such as NF-κB, which becomes activated. Cytoplasmic STAT3 dimers are activated by tyrosine phosphorylation; they interact with importins via a nuclear localization signal (NLS) one of which is located within the DNA-binding domain formed by the dimer. In the nucleus, STAT3 regulates target gene expression by binding a consensus sequence within the promoter. STAT3-specific decoy oligonucleotides (STAT3-decoy ODN) that contain this consensus sequence inhibit the transcriptional activity of STAT3, leading to cell death; however, their mechanism of action is unclear.

https://www.ncbi.nlm.nih.gov/pubmed/21486470