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Updated: Oct 26, 2025

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Head and Neck Cancer Cell Death due to Mitochondrial Damage Induced by Reactive Oxygen Species from Nonthermal

Chan Oh1, Ho-Ryun Won1,2, Woo Seok Kang3

  • 1Department of Medical Science, Chungnam National University College of Medicine, Daejeon 35015, Republic of Korea.

Oxidative Medicine and Cellular Longevity
|July 26, 2021
PubMed

Insights

Nonthermal plasma-activated media induce head and neck cancer cell death by damaging mitochondria and activating the ATF4/CHOP pathway, mimicking mitochondrial targeted therapy.

Area of Science:

  • Biochemistry
  • Oncology
  • Biophysics

Background:

  • Mitochondrial targeted therapy offers a novel approach for refractory cancers.
  • Excessive reactive oxygen species (ROS) accumulation leading to mitochondrial damage is a key principle in this therapy.
  • Nonthermal plasma-activated media (NTPAM) exhibit anticancer effects via ROS, but the precise mechanism in head and neck cancer (HNC) remains unclear.

Purpose of the Study:

  • To evaluate the anticancer effects of NTPAM on HNC cells.
  • To elucidate the signaling mechanism underlying NTPAM-induced HNC cell death.
  • To investigate the role of mitochondrial damage and ROS in this process.

Main Methods:

  • Treatment of HNC and fibroblast cell lines with NTPAM.
  • Assessment of cell viability and apoptosis.
  • Transcriptomic analysis using RNA sequencing.
  • Pathway analysis to identify key regulatory factors.

Main Results:

  • NTPAM treatment significantly decreased HNC cell viability by inducing apoptosis.
  • RNA sequencing identified 1,610 differentially expressed genes.
  • Pathway analysis revealed activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP) as upstream regulators.
  • NTPAM induced mitochondrial damage, characterized by increased mitochondrial ROS (mtROS) and upregulation of the ATF4/CHOP pathway.

Conclusions:

  • NTPAM effectively induces HNC cell death through apoptosis.
  • The mechanism involves mitochondrial damage mediated by excessive mtROS accumulation.
  • Upregulation of the ATF4/CHOP pathway is a critical event in NTPAM-induced HNC cell death, aligning with mitochondrial targeted therapy principles.

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