AI Article Synopsis
- Methylation is a key process that controls gene expression, and 5-aza-2'-deoxycytidine is a cancer treatment that works by blocking an enzyme involved in this process.
- The study indicates that long-term use of this drug can lead to problems in centrosomes of cancer cells and shows that a protein called CEP131, which is affected by the blocked enzyme, plays a role in this issue.
- Inhibiting CEP131 reduced cancer cell growth and made cells more sensitive to DNMT1 inhibitors, suggesting that targeting CEP131 could be a promising new strategy for cancer therapy.
Article Abstract
Methylation is a primary epigenetic mechanism regulating gene expression. 5-aza-2'-deoxycytidine is an FDA-approved drug prescribed for treatment of cancer by inhibiting DNA-Methyl-Transferase 1 (DNMT1). Results of this study suggest that prolonged treatment with 5-aza-2'-deoxycytidine could induce centrosome abnormalities in cancer cells and that CEP131, a centrosome protein, is regulated by DNMT1. Interestingly, cancer cell growth was attenuated in vitro and in vivo by inhibiting the expression of Cep131. Finally, Cep131-deficient cells were more sensitive to treatment with DNMT1 inhibitors. These findings suggest that Cep131 is a potential novel anti-cancer target. Agents that can inhibit this protein may be useful alone or in combination with DNMT1 inhibitors to treat cancer. [BMB Reports 2019; 52(5): 342-347].
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6549914 | PMC |
| http://dx.doi.org/10.5483/BMBRep.2019.52.5.055 | DOI Listing |
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