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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Related Experiment Video

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Assessment of Mitochondrial Health in Cancer-Associated Fibroblasts Isolated from 3D Multicellular Lung Tumor Spheroids
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TNF-α mediates mitochondrial uncoupling and enhances ROS-dependent cell migration via NF-κB activation in liver

L Kastl1, S W Sauer2, T Ruppert2

  • 1Division of Immunogenetics, Tumour Immunology Program, German Cancer Research Center (DKFZ), Heidelberg, Germany.

FEBS Letters
|December 10, 2013
PubMed
Summary

Tumor necrosis factor-alpha (TNF-α) stimulates liver cells, causing mitochondria to produce reactive oxygen species (ROS). This ROS production activates NF-κB signaling, significantly enhancing cell migration in hepatocellular carcinoma development.

Keywords:
CCCPH(2)DCF-DAHBVHCVHepatocellular carcinoma (HCC)HepatocytesLiver cancerMitochondriaN-acetylcysteineNACNF-κBROSReactive oxygen species (ROS)TMRETNF-αcarbonyl cyanide m-chlorophenyl hydrazinedichlorofluorescein diacetatehepatitis B virushepatitis C virusreactive oxygen speciestetramethylrhodamine ethyl estertumor necrosis factor-alpha

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Oncology

Background:

  • Hepatocellular carcinoma (HCC) development is linked to increased reactive oxygen species (ROS).
  • Identifying the source of ROS in liver cells is crucial for understanding HCC progression.

Purpose of the Study:

  • To determine the primary source of ROS in liver cells upon tumor necrosis factor-alpha (TNF-α) stimulation.
  • To elucidate the signaling pathways linking ROS production to cellular changes in HCC.

Main Methods:

  • Utilized TNF-α as a stimulus in liver cells.
  • Employed inhibitors targeting respiratory chain complexes to pinpoint ROS generation sites.
  • Measured mitochondrial membrane potential, ATP levels, NF-κB activation, and cell migration.

Main Results:

  • Mitochondria were identified as the primary source of ROS production induced by TNF-α.
  • TNF-α caused mitochondrial uncoupling, reducing membrane potential by 40% and ATP by 35%.
  • ROS production activated NF-κB 3.5-fold, leading to a 12.7-fold increase in cell migration.

Conclusions:

  • Complex I and Complex III of the mitochondrial respiratory chain are key sites of ROS release upon TNF-α stimulation.
  • TNF-α-induced ROS production enhances hepatocellular carcinoma cell migration via NF-κB activation.