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D-501036, a novel selenophene-based triheterocycle derivative, exhibits potent in vitro and in vivo antitumoral activity which involves DNA damage and ataxia telangiectasia-mutated nuclear protein kinase activation

  • Shin Hun Juang
  • , Chia Chi Lung
  • , Pi Chen Hsu
  • , Kuo Shun Hsu
  • , Yu Chen Li
  • , Pao Chiung Hong
  • , Her Shyong Shiah
  • , Ching Chuan Kuo
  • , Ching Wei Huang
  • , Yu Chin Wang
  • , Leeyuan Huang
  • , Tom S. Chen
  • , Shyh Fong Chen
  • , Kuo Chu Fu
  • , Cheng Li Hsu
  • , Meng Ju Lin
  • , Ching Jer Chang
  • , Curtis L. Ashendel
  • , Thomas C.K. Chan
  • , Kai Ming Chou
  • Jang Chang Chang

研究成果: 雜誌貢獻文章同行評審

66   !!Link opens in a new tab 引文 斯高帕斯(Scopus)

摘要

D-501036 [2,5-bis(5-hydroxymethyl-2-selenienyl)-3-hydroxymethyl-N-methylpyrrole] is herein identified as a novel antineoplastic agent with a broad spectrum of antitumoral activity against several human cancer cells and an IC50 value in the nanomolar range. The IC50 values for D-501036 in the renal proximal tubule, normal bronchial epithelial, and fibroblast cells were > 10 μmol/L. D-501036 exhibited no cross-resistance with vincristine- and paclitaxel-resistant cell lines, whereas a low level of resistance toward the etoposide-resistant KB variant was observed. Cell cycle analysis established that D-501036 treatment resulted in a dose-dependent accumulation in S phase with concomitant loss of both the G0-G1 and G2-M phase in both Hep 3B and A-498 cells. Pulsed-field gel electrophoresis showed D-501036-induced, concentration-dependent DNA breaks in both Hep 3B and A-498 cells. These breaks did not involve interference with either topoisomerase-I and topolsomerase-II function or DNA binding. Rapid reactive oxygen species production and formation of Se-DNA adducts were evident following exposure of cells to D-501036, indicating that D-501036 - mediated DNA breaks were attributable to the induction of reactive oxygen species and DNA adduct formation. Moreover, D-501036 - induced DNA damage activated ataxia telangiectasia - mutated nuclear protein kinase, leading to hyperphosphorylation of Chk1, Chk2, and p53, decreased expression of CDC25A, and up-regulation of p2lWAF1 in both p53-proficient and p53-deficient cells. Collectively, the results indicate that D-501036-induced cell death was associated with DNA damage - mediated induction of ataxia telangiectasia - mutated activation, and p53-dependent and -independent apoptosis pathways. Notably, D-501036 shows potent activity against the growth of xenograft tumors of human renal carcinoma A-498 cells. Thus, D-501036 is a promising anticancer compound that has strong potential for the management of human cancers.
原文英語
頁(從 - 到)193-202
頁數10
期刊Molecular Cancer Therapeutics
6
發行號1
DOIs
出版狀態已發佈 - 1月 1 2007
對外發佈

UN SDG

此研究成果有助於以下永續發展目標

  1. SDG 3 - 良好的健康和福祉
    SDG 3 良好的健康和福祉

ASJC Scopus subject areas

  • 腫瘤科
  • 癌症研究

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