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Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition

Milan Esner1, Dmitry Graifer2, Matilde E Lleonart3

  • 1Department of Histology and Embryology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.

Cancer Letters
|November 7, 2016
PubMed

Insights

Antibiotics can disrupt mitochondria, causing mitochondrial dysfunction (MDF) in both cancer and non-cancer cells. Combining autophagy inhibition with antibiotics shows promise for reducing cancer cell survival and repopulation.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Mitochondria, originating from bacteria, are susceptible to antibiotics.
  • Antibiotics are commonly used in cell culture and for genetic manipulation.
  • Targeting mitochondria with antibiotics is explored as a potential anticancer strategy.

Purpose of the Study:

  • To investigate the effects of various antibiotic classes on mitochondria in cancer and non-cancer cells.
  • To evaluate the impact of antibiotics on cancer cell survival and tumorigenic properties.
  • To explore the potential of combined antibiotic and autophagy inhibition therapy.

Main Methods:

  • Treatment of cancer and non-cancer cells with various classes of antibiotics.
  • Assessment of mitochondrial function, including membrane potential, ATP production, morphology, and respiration.
  • Measurement of reactive oxygen species (ROS) levels and mitochondrial respiration complex activity.
  • Evaluation of cancer cell survival, repopulation, and tumorigenic properties.
  • Inhibition of autophagy in conjunction with antibiotic treatment.

Main Results:

  • Antibiotics induced mitochondrial dysfunction (MDF), characterized by decreased mitochondrial membrane potential, reduced ATP production, altered morphology, and lowered respiration.
  • Increased reactive oxygen species (ROS) levels and decreased mitochondrial respiration complex activity were observed.
  • Cancer cell survival and repopulation were not significantly affected by antibiotics alone, potentially due to metabolic shifts or autophagy.
  • Simultaneous inhibition of autophagy and antibiotic treatment significantly reduced cancer cell tumorigenic properties.

Conclusions:

  • Antibiotics induce mitochondrial dysfunction (MDF) and increase ROS in both cancer and non-cancer cells.
  • Cancer cells may resist antibiotic-induced mitochondrial damage through metabolic adaptation or autophagy.
  • Combining autophagy inhibition with antibiotic therapy presents a potential strategy to enhance anticancer efficacy.
Keywords:
AntibioticsAutophagyCancerMitochondriaMitochondrial dysfunctionMitophagy

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