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

8 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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@article{4ec730849f084939b572174d7134f17c,

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",

issn = "0304-3835",

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number = "1",

}

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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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M3 - Article

C2 - 21684680

AN - SCOPUS:79959836483

SN - 0304-3835

VL - 309

SP - 110

EP - 118

JO - Cancer Letters

JF - Cancer Letters

IS - 1

ER -

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

Abstract

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