Administration sequence-dependent antitumor effects of paclitaxel and 5-fluorouracil in the human gastric cancer cell line MKN45

Cancer Chemother Pharmacol. 2006 Feb;57(3):368-75. doi: 10.1007/s00280-005-0057-9. Epub 2005 Aug 2.

Abstract

Background: The clinical outcome of gastric cancer patients has been improved by combination of 5-fluorouracil (5-FU) and paclitaxel (PXL). However, the optimal schedule of this combination has not been determined.

Methods: The efficacies of sequential administrations of 5-FU and PXL on the gastric cancer cell line MKN45 were investigated using a WST-8 colorimetric assay. The cell cycle distribution of each drug was evaluated by flow-cytometry. Furthermore, the mechanism of antitumor activity enhancement by the administration sequence was investigated by western blotting.

Results: MKN45 cell growth was significantly inhibited by each drug in a dose- and time-dependent manner. The cytotoxicities of PXL followed by 5-FU were significantly greater than those of 5-FU followed by PXL. The flow-cytometric analysis revealed that PXL exposure caused viable cell accumulation in G2/M phase in a dose-dependent manner. Western blotting showed that PXL exposure followed by 5-FU up-regulated Chk1 and Wee1 protein expressions until PXL removal and 5-FU exposure, when these expressions gradually decreased to their basal levels. 14-3-3sigma protein expression was significantly up-regulated upon PXL treatment followed by 5-FU. Interestingly, Mad2 protein expression with PXL treatment followed by 5-FU gradually increased after the PXL removal and 5-FU exposure.

Conclusions: PXL followed by 5-FU administration may be the optimal sequence for treatment of gastric cancer. The enhanced viable cell accumulation after PXL pretreatment may be related to G2 arrest. After PXL removal and 5-FU exposure, the cells progressing to M phase may undergo cell death by mitotic catastrophe due to DNA damage caused by 5-FU exposure.

Publication types

  • Comparative Study

MeSH terms

  • 14-3-3 Proteins / metabolism
  • Antimetabolites, Antineoplastic / pharmacology
  • Antineoplastic Agents, Phytogenic / pharmacology
  • Blotting, Western
  • Calcium-Binding Proteins / metabolism
  • Cell Cycle Proteins / metabolism
  • Cell Division / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Checkpoint Kinase 1
  • Dose-Response Relationship, Drug
  • Flow Cytometry / methods
  • Fluorouracil / administration & dosage
  • Fluorouracil / pharmacology*
  • G2 Phase / drug effects
  • Humans
  • Mad2 Proteins
  • Nuclear Proteins / metabolism
  • Paclitaxel / administration & dosage
  • Paclitaxel / pharmacology*
  • Protein Kinases / metabolism
  • Protein-Tyrosine Kinases / metabolism
  • Repressor Proteins / metabolism
  • Time Factors

Substances

  • 14-3-3 Proteins
  • Antimetabolites, Antineoplastic
  • Antineoplastic Agents, Phytogenic
  • Calcium-Binding Proteins
  • Cell Cycle Proteins
  • MAD2L1 protein, human
  • Mad2 Proteins
  • Nuclear Proteins
  • Repressor Proteins
  • Protein Kinases
  • Protein-Tyrosine Kinases
  • WEE1 protein, human
  • CHEK1 protein, human
  • Checkpoint Kinase 1
  • Paclitaxel
  • Fluorouracil