Overexpression of folate binding protein alpha is one of the mechanism explaining the adaptation of HT29 cells to high concentration of methotrexate

Cancer Lett. 2001 Oct 10;171(2):139-45. doi: 10.1016/s0304-3835(01)00552-3.

Abstract

The human colon adenocarcinoma cell line HT29 can be adapted to 10(-7)- 10(-4) M concentrations of methotrexate (MTX). Cells adapted to 10(-4) M MTX have an enterocyte-like phenotype with DHFR gene amplification. Presently, we hypothetized that an increased expression of folate binding protein (FBP) may participate to the MTX resistance of 10(-4) MTX HT29 cells. The cDNA FBPalpha/beta-actin ratio of amplified transcripts was 4.8- and 1.5- fold higher in 10(-4) and in 10(-7) M MTX HT29 respectively, than in standard type HT29 cells. An increase of transcript level was observed when decreasing folic acid concentration. PI-PLC cleaved 7.7 times more membrane FBP in 10(-4) M than in 10(-7) M MTX and wild type HT29 cells. In contrast to 10(-7) M MTX cells, growth of 10(-4) M MTX cells was dependent on folic acid concentration and abolished at a concentration lower than 0.9 microM. In conclusion, the adaptive mechanism of HT29 cells resistant to 10(-4) M MTX is the result of the synergistic overexpression of both DHFR and FBPalpha. Overexpression of FBPalpha may be related to the enterocyte-like phenotype of the cells.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antimetabolites, Antineoplastic / pharmacology*
  • Carrier Proteins / biosynthesis*
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Cell Division / drug effects
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm
  • Folate Receptors, GPI-Anchored
  • Folic Acid / pharmacology
  • HT29 Cells / drug effects*
  • HT29 Cells / metabolism
  • HT29 Cells / physiology
  • Humans
  • Methotrexate / pharmacology*
  • Phosphatidylinositol Diacylglycerol-Lyase
  • Phosphoinositide Phospholipase C
  • Protein Binding / drug effects
  • Protein Isoforms / biosynthesis
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Receptors, Cell Surface*
  • Tetrahydrofolate Dehydrogenase / metabolism
  • Transcription, Genetic / drug effects
  • Type C Phospholipases / metabolism

Substances

  • Antimetabolites, Antineoplastic
  • Carrier Proteins
  • Folate Receptors, GPI-Anchored
  • Protein Isoforms
  • Receptors, Cell Surface
  • Folic Acid
  • Tetrahydrofolate Dehydrogenase
  • Type C Phospholipases
  • Phosphoinositide Phospholipase C
  • Phosphatidylinositol Diacylglycerol-Lyase
  • Methotrexate