Chonnam Med J.  2006 Aug;42(2):85-93.

Decoy Oligonucleotides on Which Nuclear Factor for YB-1 Bind Inhibit the Growth of Cancer Cells

Affiliations
  • 1Division of Gastroenterology, Department of Internal Medicine, Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, Korea. bashin@chonnam.ac.kr

Abstract

Human YB-1 is a transcription factor binding on the inverted CCAAT box in the promoter region of various genes such as PCNA, DNA polymerase and MDR genes. We previously reported that the YB-1 decoy oligo deoxynucleotides (ODNs) prevent the binding of specific transcription factors on YB-1 gene. In this study we investigated the effect of the YB-1 decoy ODNs on tumor cell growth. The YB-1 decoy ODNs suppressed the proliferation of the immortalized liver cells (Chang liver cells) and various cancer cells (Hep G2, CT-26 and HeLa cells). But the normal cell growth was not altered by the YB-1 decoy ODNs treatment. The YB-1 decoy ODNs decreased the specific expression of the YB-1 mRNA in the immortalized and cancer cells as determined as Northern blot analysis. However, the YB-1 mRNA expression was not changed in normal cells. Flow cytometric analysis showed that the YB-1 decoy ODNs decreased the number of S-phase cells. This result suggest that the inhibitory effect of the YB-1 decoy ODNs on tumor cell growth depends on the reducion of the DNA synthesis in cell cycle. Furthermore, systemic or local administration of the YB-1 decoy ODNs significantly reduced the tumor volume size in animal model. These results suggest that the YB-1 decoy ODNs could inhibit the cancer cell growth via blocking of the YB-1 gene expression.

Keyword

YB-1; Decoy; Oligo deoxynucleotides; Tumor; Cell growth

MeSH Terms

Blotting, Northern
Cell Cycle
DNA
Gene Expression
Genes, MDR
Humans
Liver
Models, Animal
Oligonucleotides*
Proliferating Cell Nuclear Antigen
Promoter Regions, Genetic
RNA, Messenger
Transcription Factors
Tumor Burden
DNA
Oligonucleotides
Proliferating Cell Nuclear Antigen
RNA, Messenger
Transcription Factors
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