Growth inhibition of human hepatocellular carcinoma cells by blocking STAT3 activation with decoy-ODN.

More and more studies show that signal transducer and activator of transcription 3 (STAT3) is frequently constitutively activated in a wide number of malignancies and named as an attractive molecular target for tumor treatment. Here, we employed STAT3-decoy ODN, which specifically block over-activated STAT3, to treat human hepatocellular carcinoma (HCC) cells, and evaluated the cellular proliferation ability and investigated the molecular mechanisms in vitro. The results demonstrated that the proliferation of HCC cells was suppressed significantly by STAT3-decoy ODN, being associated with the increased apoptosis and cell arrest at G0/G1 to S phase transition. Further investigates showed the expression of STAT3-regulated genes including bcl-x1, cyclin D1 and c-myc, which involved in cell apoptosis and cell cycle progression, were down-regulated significantly both at transcription and translation levels. These data suggested that STAT3 may be potentially used as a molecular target in HCC therapy.
AuthorsXiaoxia Sun, Jian Zhang, Lihua Wang, Zhigang Tian
JournalCancer letters (Cancer Lett) Vol. 262 Issue 2 Pg. 201-13 (Apr 18 2008) ISSN: 0304-3835 [Print] Ireland
PMID18248786 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Oligodeoxyribonucleotides
  • Oligodeoxyribonucleotides, Antisense
  • STAT3 Transcription Factor
  • Apoptosis (drug effects)
  • Carcinoma, Hepatocellular (genetics)
  • Cell Cycle (drug effects)
  • Cell Line, Tumor
  • Cell Proliferation (drug effects)
  • Humans
  • Liver Neoplasms (genetics)
  • Oligodeoxyribonucleotides (pharmacology)
  • Oligodeoxyribonucleotides, Antisense (pharmacology)
  • STAT3 Transcription Factor (physiology)
  • Transcriptional Activation (drug effects)
  • Transfection

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