A forward genetic approach for analyzing the mechanism of resistance to the anti-cancer drug, 5-fluorouracil, using Caenorhabditis elegans

Mol Cells. 2008 Feb 29;25(1):119-23.

Abstract

Pyrimidine antagonists including 5-Fluorouracil (5-FU) have been used in chemotherapy for cancer patients for over 40 years. 5-FU, especially, is a mainstay treatment for colorectal cancer. It is a pro-drug that is converted to the active drug via the nucleic acid biosynthetic pathway. The metabolites of 5-FU inhibit normal RNA and DNA function, and induce apoptosis of cancer cells. One of the major obstacles to successful chemotherapy is the resistance of cancer cells to anti-cancer drugs. Therefore, it is important to elucidate resistance mechanisms to improve the efficacy of chemotherapy. We have used C. elegans as a model system to investigate the mechanism of resistance to 5-FU, which induces germ cell death and inhibits larval development in C. elegans. We screened 5-FU resistant mutants no longer arrested as larvae by 5-FU. We obtained 18 mutants out of 72,000 F1 individuals screened, and mapped them into three complementation groups. We propose that C. elegans could be a useful model system for studying mechanisms of resistance to anti-cancer drugs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antimetabolites, Antineoplastic / metabolism*
  • Antimetabolites, Antineoplastic / therapeutic use
  • Apoptosis / physiology
  • Caenorhabditis elegans / anatomy & histology
  • Caenorhabditis elegans / embryology
  • Caenorhabditis elegans / physiology*
  • Drug Resistance, Neoplasm / physiology*
  • Fluorouracil / metabolism*
  • Fluorouracil / therapeutic use
  • Genetic Complementation Test
  • Genetic Linkage
  • Germ Cells / cytology
  • Germ Cells / physiology
  • Humans
  • Neoplasms* / drug therapy
  • Neoplasms* / metabolism
  • Neoplasms* / pathology

Substances

  • Antimetabolites, Antineoplastic
  • Fluorouracil