Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer.
By: Dong Hyun Kim, Hye-Min Kim, Pham Thi Thu Huong, Ho-Jin Han, Joonsung Hwang, Hyunjoo Cha-Molstad, Kyung Ho Lee, In-Ja Ryoo, Kyoon Eon Kim, Yang Hoon Huh, Jong Seog Ahn, Yong Tae Kwon, Nak-Kyun Soung, Bo Yeon Kim

Anticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea; Department of Bio-Molecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (UST), Daejeon, 34113, Korea.
2019-5-10; doi:
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.





PMID:31068247






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