Enhancement of non-homologous end joining DNA repair capacity confers cancer cells resistance to the novel selenophene compound, D-501036

Yung Ning Yang; Kai ming Chou; Wen Yu Pan; Yih wen Chen; Tsui Chun Tsou; Ssu Ching Yeh; Chun Hei Antonio Cheung; Li Tzong Chen; Jang Yang Chang

doi:10.1016/j.canlet.2011.05.023

Enhancement of non-homologous end joining DNA repair capacity confers cancer cells resistance to the novel selenophene compound, D-501036

Yung Ning Yang, Kai ming Chou, Wen Yu Pan, Yih wen Chen, Tsui Chun Tsou, Ssu Ching Yeh, Chun Hei Antonio Cheung, Li Tzong Chen, Jang Yang Chang

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

D-501036 is a promising anti-cancer compound that exhibits potent anti-proliferative activity against various types of human cancers through the induction of double strand DNA breaks. To determine drug resistance mechanism related to this class of DNA-damaging agents, a KB-derived D-501036-resistant cell line (S4) was established. Results showed that S4 cells exhibit enhanced DNA rejoining ability as compare to KB cells, through up-regulation of the non-homologous end joining activity. In conclusion, enhancement of NHEJ activity plays important role in the development of D-501036-resistance and targeting NHEJ-related molecules maybe able to overcome drug resistance to DNA damaging agents.

Original language	English
Pages (from-to)	110-118
Number of pages	9
Journal	Cancer Letters
Volume	309
Issue number	1
DOIs	https://doi.org/10.1016/j.canlet.2011.05.023
Publication status	Published - 2011 Oct 1

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

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10.1016/j.canlet.2011.05.023

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title = "Enhancement of non-homologous end joining DNA repair capacity confers cancer cells resistance to the novel selenophene compound, D-501036",

abstract = "D-501036 is a promising anti-cancer compound that exhibits potent anti-proliferative activity against various types of human cancers through the induction of double strand DNA breaks. To determine drug resistance mechanism related to this class of DNA-damaging agents, a KB-derived D-501036-resistant cell line (S4) was established. Results showed that S4 cells exhibit enhanced DNA rejoining ability as compare to KB cells, through up-regulation of the non-homologous end joining activity. In conclusion, enhancement of NHEJ activity plays important role in the development of D-501036-resistance and targeting NHEJ-related molecules maybe able to overcome drug resistance to DNA damaging agents.",

author = "Yang, {Yung Ning} and Chou, {Kai ming} and Pan, {Wen Yu} and Chen, {Yih wen} and Tsou, {Tsui Chun} and Yeh, {Ssu Ching} and Cheung, {Chun Hei Antonio} and Chen, {Li Tzong} and Chang, {Jang Yang}",

note = "Funding Information: This study was supported by Grants of National Science Council ( NSC98-2323-B-400-004 and NSC99-2120-M-006-005 ), and Department of Health ( DOH99-TD-C-111-004 ), Taiwan, ROC. K.-M. Chou is supported by National Institutes of Health (NIH) Grant RO1 CA112446.",

year = "2011",

month = oct,

day = "1",

doi = "10.1016/j.canlet.2011.05.023",

language = "English",

volume = "309",

pages = "110--118",

journal = "Cancer Letters",

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T1 - Enhancement of non-homologous end joining DNA repair capacity confers cancer cells resistance to the novel selenophene compound, D-501036

AU - Yang, Yung Ning

AU - Chou, Kai ming

AU - Pan, Wen Yu

AU - Chen, Yih wen

AU - Tsou, Tsui Chun

AU - Yeh, Ssu Ching

AU - Cheung, Chun Hei Antonio

AU - Chen, Li Tzong

AU - Chang, Jang Yang

N1 - Funding Information: This study was supported by Grants of National Science Council ( NSC98-2323-B-400-004 and NSC99-2120-M-006-005 ), and Department of Health ( DOH99-TD-C-111-004 ), Taiwan, ROC. K.-M. Chou is supported by National Institutes of Health (NIH) Grant RO1 CA112446.

PY - 2011/10/1

Y1 - 2011/10/1

N2 - D-501036 is a promising anti-cancer compound that exhibits potent anti-proliferative activity against various types of human cancers through the induction of double strand DNA breaks. To determine drug resistance mechanism related to this class of DNA-damaging agents, a KB-derived D-501036-resistant cell line (S4) was established. Results showed that S4 cells exhibit enhanced DNA rejoining ability as compare to KB cells, through up-regulation of the non-homologous end joining activity. In conclusion, enhancement of NHEJ activity plays important role in the development of D-501036-resistance and targeting NHEJ-related molecules maybe able to overcome drug resistance to DNA damaging agents.

AB - D-501036 is a promising anti-cancer compound that exhibits potent anti-proliferative activity against various types of human cancers through the induction of double strand DNA breaks. To determine drug resistance mechanism related to this class of DNA-damaging agents, a KB-derived D-501036-resistant cell line (S4) was established. Results showed that S4 cells exhibit enhanced DNA rejoining ability as compare to KB cells, through up-regulation of the non-homologous end joining activity. In conclusion, enhancement of NHEJ activity plays important role in the development of D-501036-resistance and targeting NHEJ-related molecules maybe able to overcome drug resistance to DNA damaging agents.

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Enhancement of non-homologous end joining DNA repair capacity confers cancer cells resistance to the novel selenophene compound, D-501036

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