ArticleInternational journal of oncology2010
Enhanced growth inhibition by combined DNA methylation/HDAC inhibitors in lung tumor cells with silenced CDKN2A.
Article in International journal of oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
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- CDK4/6 inhibition stabilizes disease in patients with p16-null non-small cell lung cancer and is synergistic with mTOR inhibition.Oncotarget · 2018Article
- Comparison of DNA demethylating and histone deacetylase inhibitors hydralazine-valproate versus vorinostat-decitabine incutaneous t-cell lymphoma in HUT78 cells.American journal of blood research · 2018Article
- Targeting Histone Deacetylases in Diseases: Where Are We?Antioxidants & redox signaling · 2015Review
- Article
- Nrf2 status affects tumor growth, HDAC3 gene promoter associations, and the response to sulforaphane in the colon.Clinical epigenetics · 2015Article
- A specific missense mutation in GTF2I occurs at high frequency in thymic epithelial tumors.Nature genetics · 2014Article
- Achieving a cure for HIV infection: do we have reasons to be optimistic?The Journal of antimicrobial chemotherapy · 2012Review
- DNA methyltransferase inhibitor, zebularine, delays tumor growth and induces apoptosis in a genetically engineered mouse model of breast cancer.Molecular cancer therapeutics · 2012Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant hypermethylation at CpG sites within the CDKN2A gene is associated with silencing and has been proposed as a target for reactivation using both DNA methylation and histone deacetylation inhibitors. This study investigates the role of selecting tumor samples with a silenced as compared to deleted CDKN2A locus when assessing the efficacy of DNA methyltransferase inhibitor, zebularine, combined with the HDAC inhibitor, depsipeptide. Non-small cell lung cancer cell lines with defined CDKN2A status were analyzed by MTS assay to determine the effect of zebularine or zebularine combined with depsipeptide on tumor cell growth. We observed that zebularine treatment resulted in inhibition of cell growth in 11 out of 12 lung cancer cell lines with silenced CDKN2A, but no cell growth inhibition was detected in the 7 lung cancer cell lines tested with deleted CDKN2A (p>0.001). In addition, we found that the combination of 30 microM zebularine and 6 or 7 nM depsipeptide resulted in a synergistic inhibition of cell growth in tumor cells with silenced CDKN2A (p<0.001, CI=0.70 and 0.57, respectively) but not in tumor cells with deleted CDKN2A. In conclusion, tumor cells with methylated CDKN2A are more sensitive to zebularine than cell lines with deleted CDKN2A and the combination of zebularine/depsipeptide results in a synergistic effect on cell growth inhibition that is also linked with the presence of silenced CDKN2A. Thus, combination of DNA methyltransferase and HDAC inhibitors may be a potential treatment for lung cancer patients, but careful selection of patients will be needed to optimize the benefit of this regimen.
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