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Published on: March 8, 2012
Antisense oligodeoxynucleotides to c-jun inhibits proliferation of transformed NIH 3T3 cells induced by E5a of HPV-11
1Department of Microbiology and Immunology National Defense Medical Center, Taipei, Taiwan, ROC.
Abstract:
E5a of HPV-11 is a transforming oncogene. Previously, we had shown that the E5a gene is required only for the initiation of transformation; c-jun might be involved in the maintenance of transformation. In this study, we exposed E5a transformed NIH 3T3 cells to antisense oligodeoxynucleotides complementary to the 24 nucleotides corresponding to the translation initiation site of the c-jun gene, and examined the effects of this treatment on cell proliferation. Results show that antisense c-jun oligodeoxynucleotides could repress c-jun production and inhibit cell proliferation in E5a transformed cells.
Insights
Human papillomavirus type 11 (HPV-11) E5a oncogene drives cell transformation. This study shows that inhibiting c-jun production with antisense oligodeoxynucleotides halts proliferation in E5a-transformed cells.
Area of Science:
- Oncogenomics
- Molecular Virology
Background:
- The E5a gene of Human Papillomavirus type 11 (HPV-11) is a transforming oncogene.
- Previous research indicated E5a's role in initiating cell transformation, with c-jun potentially involved in maintaining this state.
Purpose of the Study:
- To investigate the role of c-jun in the maintenance of E5a-mediated cell transformation.
- To determine the effect of inhibiting c-jun production on the proliferation of E5a-transformed cells.
Main Methods:
- NIH 3T3 cells transformed by HPV-11 E5a were treated with antisense oligodeoxynucleotides.
- These oligodeoxynucleotides were designed to be complementary to the translation initiation site of the c-jun gene.
- Cell proliferation was monitored following the treatment.
Main Results:
- Antisense c-jun oligodeoxynucleotides successfully repressed the production of c-jun protein.
- This repression of c-jun led to a significant inhibition of cell proliferation in E5a-transformed NIH 3T3 cells.
Conclusions:
- c-jun plays a crucial role in maintaining the transformed phenotype induced by HPV-11 E5a.
- Targeting c-jun production offers a potential therapeutic strategy for HPV-11-associated cancers.
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