Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer
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- Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer
- Dong Hyun Kim; Hye-Min Kim; P T T Huong; Ho Jin Han; Joonsung Hwang; Hyunjoo Cha; Kyung Ho Lee; In Ja Ryoo; K E Kim; Y H Huh; Jong Seog Ahn; Y T Kwon; Nak Kyun Soung; Bo Yeon Kim
- Bibliographic Citation
- BMB Reports, vol. 52, no. 5, pp. 342-347
- Publication Year
- 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.
- Anti-cancer; Centrosome; CEP131; DNMT1
- South Korea
- Appears in Collections:
- Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
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