Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer

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...

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Published in:BMB reports 2019, 52(5), , pp.342-347
Main Authors: Kim, Dong Hyun, Kim, Hye-Min, Huong, Pham Thi Thu, Han, Ho-Jin, Hwang, Joonsung, Cha-Molstad, Hyunjoo, Lee, Kyung Ho, Ryoo, In-Ja, Kim, Kyoon Eon, Huh, Yang Hoon, Ahn, Jong Seog, Kwon, Yong Tae, Soung, Nak-Kyun, Kim, Bo Yeon
Format: Article
Language:English
Subjects:
화학
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Summary: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.
ISSN:1976-6696
1976-670X
DOI:10.5483/BMBRep.2019.52.5.055