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ISG12a mediates cell response to Newcastle disease viral infection

Nianli Liu1, Ying Long2, Bin Liu2

  • 1Department of Molecular Medicine, State Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha 410082, China; Research Center of Cancer Prevention & Treatment, Translational Medicine Research Center of Liver Cancer, Hunan Provincial Tumor Hospital (Affiliated Tumor Hospital of Xiangya Medical School of Central South University), Changsha 410013, China.

Virology
|July 8, 2014
PubMed

Insights

Newcastle disease virus (NDV) oncolysis in cancer cells depends on interferon responses. Low interferon-stimulated gene 12a (ISG-12a) levels promote NDV oncolysis, suggesting therapeutic potential.

Area of Science:

  • Virology
  • Immunology
  • Oncology

Background:

  • Newcastle disease virus (NDV) is a promising oncolytic virus, with its efficacy potentially linked to the host's Type I interferon (IFN) response.
  • Hepatocellular carcinoma (HCC) is a major global health concern, and understanding viral oncolysis mechanisms in HCC is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the role of Type I interferon response, specifically interferon-stimulated gene 12a (ISG-12a), in Newcastle disease virus (NDV) oncolysis of hepatocellular carcinoma (HCC) cells.
  • To compare the susceptibility of TRAIL-resistant and TRAIL-sensitive HCC cells to NDV oncolysis and elucidate the underlying IFN-related mechanisms.

Main Methods:

  • Comparative analysis of TRAIL-resistant and TRAIL-sensitive HCC cell lines.
  • Assessment of NDV replication and oncolysis.
  • Investigation of basal and induced expression of ISG-12a.
  • Manipulation of ISG-12a expression (over-expression and silencing).
  • Evaluation of the roles of RIG-I and Noxa in NDV oncolysis.

Main Results:

  • TRAIL-resistant HCC cells, with lower basal ISG-12a expression, were more susceptible to NDV oncolysis than TRAIL-sensitive cells.
  • Over-expression of ISG-12a in TRAIL-resistant cells reduced NDV replication but enhanced oncolysis, while ISG-12a silencing in TRAIL-sensitive cells had opposite effects.
  • RIG-I and Noxa were identified as contributing factors to NDV oncolysis.

Conclusions:

  • Basal levels of ISG-12a significantly influence NDV oncolysis, with low levels promoting viral replication and subsequent oncolysis.
  • ISG-12a modulation presents a potential therapeutic strategy to enhance NDV oncolysis in HCC.
  • The interplay between IFN response, viral replication, and cell death pathways is critical for effective oncolytic virotherapy.
Keywords:
ISG12aInnate immunityLiver cancerNewcastle disease virus

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