Fractal analysis and ionic dependence of endocytotic membrane activity of human breast cancer cells

Eur Biophys J. 2009 Oct;38(8):1115-25. doi: 10.1007/s00249-009-0516-z. Epub 2009 Jul 18.


The endocytic membrane activities of two human breast cancer cell lines (MDA-MB-231 and MCF-7) of strong and weak metastatic potential, respectively, were studied in a comparative approach. Uptake of horseradish peroxidase was used to follow endocytosis. Dependence on ionic conditions and voltage-gated sodium channel (VGSC) activity were characterized. Fractal methods were used to analyze quantitative differences in vesicular patterning. Digital quantification showed that MDA-MB-231 cells took up more tracer (i.e., were more endocytic) than MCF-7 cells. For the former, uptake was totally dependent on extracellular Na(+) and partially dependent on extracellular and intracellular Ca(2+) and protein kinase activity. Analyzing the generalized fractal dimension (D(q )) and its Legendre transform f(alpha) revealed that under control conditions, all multifractal parameters determined had values greater for MDA-MB-231 compared with MCF-7 cells, consistent with endocytic/vesicular activity being more developed in the strongly metastatic cells. All fractal parameters studied were sensitive to the VGSC blocker tetrodotoxin (TTX). Some of the parameters had a "simple" dependence on VGSC activity, if present, whereby pretreatment with TTX reduced the values for the MDA-MB-231 cells and eliminated the differences between the two cell lines. For other parameters, however, there was a "complex" dependence on VGSC activity. The possible physical/physiological meaning of the mathematical parameters studied and the nature of involvement of VGSC activity in control of endocytosis/secretion are discussed.

Publication types

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

MeSH terms

  • Breast Neoplasms / pathology
  • Breast Neoplasms / physiopathology*
  • Cell Line, Tumor
  • Cell Membrane*
  • Endocytosis*
  • Fractals
  • Humans
  • Ion Channel Gating*
  • Sodium Channels / metabolism*


  • Sodium Channels