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 Cheung, Li Tzong Chen, Jang-Yang Chang

Research output: Contribution to journalArticle

5 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 languageEnglish
Pages (from-to)110-118
Number of pages9
JournalCancer Letters
Volume309
Issue number1
DOIs
Publication statusPublished - 2011 Oct 1

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DNA Repair
Drug Resistance
DNA
KB Cells
Neoplasms
Double-Stranded DNA Breaks
Up-Regulation
Cell Line
2,5-bis(5-hydroxymethyl-2-selenienyl)-3-hydroxymethyl-N-methylpyrrole

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Yang, Yung Ning ; Chou, Kai ming ; Pan, Wen Yu ; Chen, Yih wen ; Tsou, Tsui Chun ; Yeh, Ssu Ching ; Cheung, Chun-Hei ; Chen, Li Tzong ; Chang, Jang-Yang. / Enhancement of non-homologous end joining DNA repair capacity confers cancer cells resistance to the novel selenophene compound, D-501036. In: Cancer Letters. 2011 ; Vol. 309, No. 1. pp. 110-118.
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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.",
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Enhancement of non-homologous end joining DNA repair capacity confers cancer cells resistance to the novel selenophene compound, D-501036. / Yang, Yung Ning; Chou, Kai ming; Pan, Wen Yu; Chen, Yih wen; Tsou, Tsui Chun; Yeh, Ssu Ching; Cheung, Chun-Hei; Chen, Li Tzong; Chang, Jang-Yang.

In: Cancer Letters, Vol. 309, No. 1, 01.10.2011, p. 110-118.

Research output: Contribution to journalArticle

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