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Doxycycline Impairs Mitochondrial Function and Protects Human Glioma Cells from Hypoxia-Induced Cell Death:

Anna-Luisa Luger1,2, Benedikt Sauer3,4, Nadja I Lorenz5,6

  • 1Dr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, Schleusenweg 2-16, 60528 Frankfurt am Main, Germany. Anna-Luisa.Luger@kgu.de.

International Journal of Molecular Sciences
|May 19, 2018
PubMed

Insights

Doxycycline, used in tetracycline-inducible systems, significantly alters cancer cell metabolism even at low doses. This impacts mitochondrial function and energy use, potentially limiting its research applications.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Metabolism

Background:

  • Tetracycline (Tet)-inducible systems are crucial for studying protein function via inducible gene expression.
  • Doxycycline is commonly used in Tet-inducible systems, but concerns exist regarding its impact on mitochondrial function and cellular metabolism.
  • Metabolic reprogramming is a key hallmark of cancer, making its study critical in cancer research.

Purpose of the Study:

  • To systematically analyze the dose-dependent metabolic effects of doxycycline on glioma cell lines.
  • To monitor gene expression from Tet-inducible systems concurrently with metabolic changes.
  • To assess the impact of doxycycline on cellular metabolism in the context of cancer research.

Main Methods:

  • Dose-dependent analysis of doxycycline on glioma cell lines.
  • Monitoring of gene expression from Tet-inducible systems.
  • Measurement of cellular metabolic parameters, including oxygen consumption and glucose uptake.
  • Assessment of cell viability and growth under varying doxycycline concentrations and hypoxia.

Main Results:

  • Doxycycline at commonly used concentrations (0.01–1 µg/mL) significantly alters cellular metabolism.
  • Inhibition of mitochondrial protein synthesis, reduced oxygen consumption, and increased glucose consumption were observed.
  • Doxycycline demonstrated a protective effect on human glioma cells against hypoxia-induced cell death.
  • Impaired cell growth was only observed at higher doxycycline doses (10 µg/mL).

Conclusions:

  • Doxycycline exerts significant metabolic effects on eukaryotic cells at doses relevant to inducible gene expression systems.
  • These findings highlight potential limitations in using Tet-inducible systems due to doxycycline's interference with cellular metabolism.
  • Researchers should carefully consider doxycycline's metabolic impact when employing Tet-inducible systems, especially in cancer metabolism studies.
Keywords:
Tet-inducible systemdoxycyclineglioblastomahypoxia-induced cell deathinducible gene expressionmitochondriatetracyclinetumor metabolism

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