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The STAT-ROS cycle extends IFN‑induced cancer cell apoptosis

Yan Wang1, Xiaoyu Yu1, Hongtao Song1

  • 1Department of Pathology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang 150081, P.R. China.

International Journal of Oncology
|November 9, 2017
PubMed

Insights

A novel STAT-ROS cycle enhances interferon-induced cancer cell apoptosis. This cycle involves signal transducer and activator of transcription (STAT) proteins and reactive oxygen species (ROS) interacting to promote cell death.

Area of Science:

  • Cellular biology
  • Cancer research
  • Biochemistry

Background:

  • Signal transducer and activator of transcription (STAT) proteins and reactive oxygen species (ROS) are involved in cellular processes.
  • Interferon (IFN) therapy can induce cancer cell apoptosis through STAT activation and ROS accumulation.
  • The interplay between STAT and ROS, forming a potential cycle, and its role in IFN-induced apoptosis remain unclear.

Purpose of the Study:

  • To investigate the existence and function of a STAT-ROS cycle in cancer cells.
  • To determine the role of this cycle in interferon-induced cancer cell apoptosis.

Main Methods:

  • Utilized MCF7 breast cancer cells, with subsequent validation in A431 and HeLa cancer cells.
  • Employed techniques including interferon (IFN-α/β/γ) incubation, STAT1/3 overexpression and deletion, and hydrogen peroxide (H2O2) treatment.
  • Monitored STAT1/3 phosphorylation, mitochondrial import, mitochondrial respiratory complexes, oxygen consumption rate (OCR), ROS production, and cellular apoptosis.

Main Results:

  • IFN-α/β/γ induced STAT1/3 phosphorylation, mitochondrial import, increased respiratory complexes, OCR, ROS production, and apoptosis in MCF7 cells.
  • STAT1/3 overexpression enhanced mitochondrial respiratory complexes and ROS production.
  • ROS induced by H2O2 promoted STAT1/3 phosphorylation and mitochondrial import, while STAT1/3 deletion impaired H2O2-induced OCR and ROS.
  • IFN-induced apoptosis was partially blocked by STAT1/3 deletion, and ROS suppression inhibited IFN-induced STAT1/3 activation.
  • The STAT-ROS cycle was confirmed in A431 and HeLa cancer cells.

Conclusions:

  • A STAT-ROS cycle, involving mutual activation between STAT proteins and ROS, was identified.
  • This STAT-ROS cycle plays a significant role in extending interferon-induced cancer cell apoptosis.
  • The findings suggest potential therapeutic strategies targeting the STAT-ROS pathway in cancer treatment.

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