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An RNA Molecule Derived From Sendai Virus DI Particles Induces Antitumor Immunity and Cancer Cell-selective Apoptosis

Li-Wen Liu1, Tomoyuki Nishikawa1, Yasufumi Kaneda1

  • 1Division of Gene Therapy Science, Graduate School of Medicine, Osaka University, Osaka, Japan.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|November 10, 2015
PubMed

Insights

Defective-interfering particles from Sendai virus (HVJ) effectively induce prostate cancer cell death. Their RNA activates proapoptotic genes, offering a novel nucleic acid therapy for cancer treatment.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology
  • Oncology

Background:

  • Inactivated Sendai virus envelope (HVJ-E) demonstrates anticancer properties by inducing apoptosis via retinoic acid-inducible gene-I (RIG-I) recognition of viral RNA.
  • Defective-interfering (DI) particles are a specific type of viral particle that can influence viral replication and host responses.

Purpose of the Study:

  • To investigate the efficacy of "copy-back" type defective-interfering (DI) particles from Sendai virus (HVJ) in inducing cancer cell death.
  • To explore the molecular mechanisms underlying the anticancer effects of DI particle-derived RNA.
  • To evaluate the therapeutic potential of DI particle-derived RNA in a preclinical cancer model.

Main Methods:

  • Comparison of the cytotoxic effects of different HVJ strains (Cantell, Sendai/52) and isolated DI particles on human PC3 prostate cancer cells.
  • In vitro transcription (IVT) of DI particle genomic RNA (IVT-B2) and control RNA (IVT-HN) to assess their anticancer activity.
  • Intratumoral transfection of IVT-B2 in a human prostate tumor xenograft mouse model to evaluate in vivo efficacy.
  • Analysis of proapoptotic gene activation (Noxa, TRAIL) and assessment of natural killer (NK) cell involvement.

Main Results:

  • The "copy-back" DI particles from the Cantell strain of HVJ showed superior efficacy in inducing human PC3 prostate cancer cell death compared to other HVJ strains.
  • DI particle genomic RNA activated proapoptotic genes, leading to cancer cell-selective apoptosis.
  • In vitro transcribed DI particle RNA (IVT-B2), possessing a double-stranded region, exhibited a stronger anticancer effect than control RNA (IVT-HN).
  • Intratumoral administration of IVT-B2 significantly reduced tumor volume and induced apoptosis in the xenograft model, with suggested involvement of NK cells.

Conclusions:

  • "Copy-back" DI particles of HVJ possess potent cancer cell-selective apoptotic activity.
  • DI particle-derived RNA, particularly IVT-B2, represents a promising novel nucleic acid-based therapeutic agent for cancer treatment.
  • Further research into the role of NK cells may elucidate additional mechanisms of action for this novel therapy.

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