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Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
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Diabetogenic glucose and insulin concentrations modulate transcriptome and protein levels involved in tumour cell

K Masur1, C Vetter, A Hinz

  • 1Institute of Immunology and Experimental Oncology, University Witten/Herdecke, Stockumer Str. 10, Witten 58448, Germany. kai.masur@inp-greifswald.de

British Journal of Cancer
|December 24, 2010
PubMed
Abstract

Insights

High glucose and insulin levels promote cancer cell proliferation and migration by activating key signaling pathways. This study investigates the molecular mechanisms linking hyperglycemia and hyperinsulinemia to tumor growth and metastasis.

Area of Science:

  • Oncology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Epidemiological studies link metabolic syndrome and type 2 diabetes mellitus (DM T2) to increased cancer progression.
  • The precise mechanisms by which high glucose and insulin influence cancer cell gene activity and signaling pathways remain incompletely understood.

Purpose of the Study:

  • To investigate the impact of diabetogenic glucose and insulin concentrations on cancer cell proliferation and migration.
  • To elucidate how high glucose and insulin levels affect gene and signal cascade activities, focusing on kinases involved in tumor cell behavior.

Main Methods:

  • Analysis of over 400 gene signatures related to cell cycle, cell movement, and signal transduction.
  • Transcriptome analysis of kinases (PKCα, PI3K), cadherins, integrins, and cyclins under physiological (5.5 mM) versus diabetogenic (11 mM) glucose concentrations, with and without insulin.

Main Results:

  • High glucose (11 mM) and insulin (100 ng/ml) significantly promoted proliferation in multiple tumor cell lines (HT29, SW480, MCF-7, MDA MB468, PC3, T24).
  • Elevated glucose concentrations increased tumor cell motility in 3D-migration assays.
  • Increased migratory activity under high glucose and insulin was mediated by the activation of PI3K, PKCα, and MLCK, confirmed by pharmacological inhibitors.

Conclusions:

  • This study provides molecular and functional evidence for how hyperglycemia and hyperinsulinemia can drive tumor cell proliferation and motility.
  • Findings offer insights into the potential mechanisms by which metabolic dysregulation contributes to cancer progression in patients.

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