A computational multiscale model of glioblastoma growth: regulation of cell migration and proliferation via microRNA-451, LKB1 and AMPK

Annu Int Conf IEEE Eng Med Biol Soc. 2012:2012:6620-3. doi: 10.1109/EMBC.2012.6347512.

Abstract

A new computational multiscale model of glioblastoma growth is introduced. This model combines an agent-based model for representing processes on the cellular level with a molecular interaction network for each cell on the subcellular scale. The network is based on recently published work on the interaction of microRNA-451, LKB1 and AMPK in the regulation of glioblastoma cell migration and proliferation. We translated this network into a mathematical description by the use of 17 ordinary differential equations. In our model, we furthermore establish a link from the molecular interaction network of a single cell to cellular actions (e.g. chemotactic movement) on the microscopic level. First results demonstrate that the computational model reproduces a tumor cell development comparable to that observed in in vitro experiments.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinase Kinases
  • AMP-Activated Protein Kinases / metabolism*
  • Brain Neoplasms / metabolism
  • Cell Movement
  • Cell Proliferation
  • Chemotaxis
  • Computer Simulation
  • Glioblastoma / pathology*
  • Glucose / metabolism
  • Humans
  • MicroRNAs / metabolism*
  • Models, Statistical
  • Phenotype
  • Protein Serine-Threonine Kinases / metabolism*

Substances

  • MIRN451 microRNA, human
  • MicroRNAs
  • Protein Serine-Threonine Kinases
  • STK11 protein, human
  • AMP-Activated Protein Kinase Kinases
  • AMP-Activated Protein Kinases
  • Glucose