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

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, Yongtae Kwon, Nak Kyun Soung, Bo Yeon Kim

Research output: Contribution to journalComment/debateResearch

1 Citation (Scopus)

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].

Original languageEnglish
Pages (from-to)342-347
Number of pages6
JournalBMB Reports
Volume52
Issue number5
DOIs
StatePublished - 1 May 2019

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Methylation
decitabine
Transferases
Uterine Cervical Neoplasms
DNA
Centrosome
Neoplasms
Cell growth
Gene expression
Proteins
Epigenomics
Cells
Gene Expression
Pharmaceutical Preparations
Growth

Cite this

Kim, D. H., Kim, H. M., Huong, P. T. T., Han, H. J., Hwang, J., Cha-Molstad, H., ... Kim, B. Y. (2019). Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer. BMB Reports, 52(5), 342-347. https://doi.org/10.5483/bmbrep.2019.52.5.055
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, Yongtae ; Soung, Nak Kyun ; Kim, Bo Yeon. / Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer. In: BMB Reports. 2019 ; Vol. 52, No. 5. pp. 342-347.
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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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Kim, DH, Kim, HM, Huong, PTT, Han, HJ, Hwang, J, Cha-Molstad, H, Lee, KH, Ryoo, IJ, Kim, KE, Huh, YH, Ahn, JS, Kwon, Y, Soung, NK & Kim, BY 2019, 'Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer', BMB Reports, vol. 52, no. 5, pp. 342-347. https://doi.org/10.5483/bmbrep.2019.52.5.055

Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer. / 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, Yongtae; Soung, Nak Kyun; Kim, Bo Yeon.

In: BMB Reports, Vol. 52, No. 5, 01.05.2019, p. 342-347.

Research output: Contribution to journalComment/debateResearch

TY - JOUR

T1 - Enhanced anticancer effects of a methylation inhibitor by inhibiting a novel DNMT1 target, CEP 131, in cervical cancer

AU - Kim, Dong Hyun

AU - Kim, Hye Min

AU - Huong, Pham Thi Thu

AU - Han, Ho Jin

AU - Hwang, Joonsung

AU - Cha-Molstad, Hyunjoo

AU - Lee, Kyung Ho

AU - Ryoo, In Ja

AU - Kim, Kyoon Eon

AU - Huh, Yang Hoon

AU - Ahn, Jong Seog

AU - Kwon, Yongtae

AU - Soung, Nak Kyun

AU - Kim, Bo Yeon

PY - 2019/5/1

Y1 - 2019/5/1

N2 - 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].

AB - 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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M3 - Comment/debate

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EP - 347

JO - BMB reports

JF - BMB reports

SN - 1976-6696

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