Cited by 80Cytokine Signaling Pathways and InteractionsHepatocellular Carcinoma Treatment and PrognosisLiver physiology and pathology

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

Sun, Xiaoxia, Zhang, Jian, Wang, Lihua, Tian, Zhigang·2008·Cancer Letters

Abstract

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.

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Crossref · 10.1016/j.canlet.2007.12.009

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  • Nucleic acid-based drugs, including decoy oligonucleotides and, perhaps, G-quartet oligonucleotides, inhibit STAT3-mediated gene expression and inhibit growth of different cancer cell lines.

    “Nucleic acid–based drugs, including decoy oligonucleotides and, perhaps, G-quartet oligonucleotides, have been identified that inhibit STAT3-mediated gene expression and inhibit growth of different cancer cell lines (Leong et al., 2003; Lewis et al., 2008; Sun et al., 2008; Shen et al., 2009; Zhang et al., 2013b; Liu et al., 2014; Sen et al., 2014).”

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Authors
Sun, X., Zhang, J., Wang, L., & Tian, Z.
Affiliations
  • Shandong First Medical University (CN)
  • Shandong University (CN)
Corresponding author
  • Zhang, Jian
  • Tian, Zhigang
Venue
Cancer Letters
Publisher
Elsevier BV
Published
2008-04
Volume
262
Issue
2
Pages
201-213
ISSN
0304-3835 (ISSN-L)
OpenAlex
W2059069220
Cited by
80
References
4
Citations by year
2025: 3 · 2024: 3 · 2023: 3 · 2021: 1 · 2020: 4 · 2019: 2 · 2018: 1 · 2017: 5 · 2016: 6 · 2015: 8 · 2014: 7 · 2013: 5 · 2012: 6
FWCI
4.57
Type
journal article
Language
en
Open access
closed
Locations
  • Cancer Letters (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Key Research and Development Program of China
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
STAT3, hepatocellular carcinoma, decoy oligonucleotides, cell proliferation, apoptosis, G0/G1 cell cycle arrest, Bcl-xL, cyclin D1, c-Myc, transcriptional regulation, cancer therapy
MeSH terms
Cell Cycle, Carcinoma, Hepatocellular, Humans, Liver Neoplasms, Oligodeoxyribonucleotides, Transfection, Transcriptional Activation, Apoptosis, Oligodeoxyribonucleotides, Antisense, Cell Line, Tumor, Cell Proliferation, STAT3 Transcription Factor

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