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Interferon-stimulated gene 15 induces cancer cell death by suppressing the NF-κB signaling pathway

Hongwu Mao1,2, Man Wang1, Biyin Cao1

  • 1Jiangsu Key Laboratory for Translational Research and Therapeutics of Neuro-Psycho-Diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, P.R. China.

Oncotarget
|September 24, 2016
PubMed

Insights

Interferon-stimulated gene 15 (ISG15) and its de-ISGylase USP18 were found to inhibit cancer cell proliferation and induce apoptosis. ISG15 suppresses tumor growth by disrupting the NF-κB signaling pathway, highlighting its novel tumor-suppressive role.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Interferon-stimulated gene 15 (ISG15) has been implicated in carcinogenesis.
  • The role of ISG15 and its de-ISGylase USP18 in cancer progression requires further elucidation.

Purpose of the Study:

  • To investigate the role of ISG15 and USP18 in cancer.
  • To elucidate the underlying molecular mechanisms of ISG15-mediated tumor suppression.

Main Methods:

  • Reverse transcription-polymerase chain reaction (RT-PCR) and immunoblotting assays.
  • In vitro cell proliferation and apoptosis assays in myeloma, leukemia, and cervical cancer cell lines.
  • In vivo cervical cancer xenograft model.
  • Analysis of the NF-κB signaling pathway.

Main Results:

  • ISG15 and USP18 were induced by anti-cancer agents and inhibited proliferation of various cancer cells.
  • Ectopic ISG15 and USP18 induced cancer cell apoptosis, confirmed in a cervical xenograft model.
  • ISG15 disrupted the NF-κB signaling pathway by downregulating IKKβ and p65, and suppressing NF-κB-driven transcription.

Conclusions:

  • ISG15 induces cancer cell apoptosis through the disruption of the NF-κB signaling pathway.
  • ISG15 exhibits a novel tumor-suppressive role, making it a potential therapeutic target.
Keywords:
ISG15NF-κBapoptosiscancer

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