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Increased sensitivity to cytosine arabinoside in human leukemia by c-raf-1 antisense oligonucleotides

T Funato1, K Kozawa, S Fujimaki

  • 1Division of Molecular Diagnostics, Department of Clinical Medicine, Tohoku University, School of Medicine, Seiryoumachi 1-1, Aoba-ku, Sendai 980-8574, Japan. tfunato@mail.cc.tohoku.ac.jp

Anti-Cancer Drugs
|May 4, 2001
PubMed

Insights

Increased c-raf-1 expression contributes to leukemia drug resistance. Inhibiting c-raf-1 with antisense oligonucleotides enhanced sensitivity to cytosine arabinoside (Ara-C) in leukemia cells.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • c-raf-1 is a serine/threonine protein kinase involved in cellular signal transduction, growth, proliferation, and survival.
  • The role of c-raf-1 in leukemia remains unclear, despite its study in other tumors.

Purpose of the Study:

  • To investigate the expression of c-raf-1 in human leukemia cell lines.
  • To determine if inhibiting c-raf-1 enhances sensitivity to cytosine arabinoside (Ara-C) in leukemia cells.

Main Methods:

  • Examined c-raf-1 expression in U937 and K562 leukemia cell lines, including an Ara-C-resistant K562AC derivative.
  • Utilized antisense oligonucleotides to inhibit c-raf-1 expression.
  • Assessed sensitivity to Ara-C and other chemotherapeutic agents (adriamycin, VP-16, vincristine).

Main Results:

  • c-raf-1 expression was elevated in U937 and K562AC cells compared to parental cells.
  • Antisense inhibition of c-raf-1 reduced c-raf-1 mRNA levels without impacting cell growth.
  • Inhibition of c-raf-1 increased sensitivity to Ara-C but not to adriamycin, VP-16, or vincristine.

Conclusions:

  • c-raf-1 is implicated as a factor contributing to Ara-C resistance in leukemia.
  • Targeting c-raf-1 with oncogene-targeted antisense oligonucleotides shows potential for novel anti-cancer therapeutics.

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