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Anticancer effects of a methylation inhibitor are enhanced by inhibition of the novel DNMT1 target, CEP 131 in cervical cancer
Nak-Kyun Soung1,5,*, Dong Hyun Kim1,5,#, Pham Thi Thu Huong Huong1,#, Hye-Min Kim1,#, Ho-Jin Han1,5, Joonsung Hwang1, Hyunjoo Cha-Molstad1, Kyung Ho Lee1, In-Ja Ryoo1, Kyoon Eon Kim2, Yang Hoon Huh3, Jong Seog Ahn1,5, Yong Tae Kwon4, Nak-Kyun Soung1,5,*, Bo Yeon Kim1,5
1Anticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB),
2Department of Biochemistry, ChungNam National University,
3Center for Electron Microscopy Research, Korea Basic Science Institute,
4Protein Metabolism Medical Research Center, Department of Biomedical Sciences, College of Medicine, Seoul National University,
5Department of Bio-Molecular Science, KRIBB School of Bioscience, Korea University of Science and Technology (UST)
Methylation is a primary epigenetic mechanism regulating gene expression. 5-Aza-2∏-deoxycytidine is an FDA-approved drug prescribed for the treatment of inhibition of DNA-Methyl-Transferase 1 (DNMT1). The results of this study suggest that: i) prolonged treatment with 5-Aza-2∏-deoxycytidine induces centrosome abnormalities in cancer cells, and ii) 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. Based on these findings, we suggest that Cep131 is a potential novel anti-cancer target, and that agents which inhibit this protein may be investigated, perhaps in combination with DNMT1 inhibitors.
Abstract, Accepted Manuscript(in press) [Submitted on February 25, 2019, Accepted on April 9, 2019]
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