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Inhibition of human lung carcinoma cell growth by apoptosis induction using Semliki Forest virus recombinant
A M Murphy1, M M Morris-Downes, B J Sheahan
1Department of Microbiology, Moyne Institute of Preventive Medicine, Trinity College, Dublin, Ireland.
Abstract:
We have utilised cell cultures and growth of tumours in nude mice to assess further the potential of the Semliki Forest virus (SFV) vector as a cancer therapy agent. This vector is a transient RNA-based expression vector, and we have previously shown that SFV and its derived vector can induce p53-independent apoptosis by expression of the nonstructural region of the virus genome. Apoptosis induction is therefore an inherent property of the vector and is not dependent on heterologous gene expression. SFV recombinant suicide particles (rSFV) were shown to induce apoptosis in H358a cells, which are human non-small cell lung carcinoma cells deleted in p53. EGFP-expressing rSFV also inhibited the growth of developing H358a spheroids. Direct injection of rSFV into H358a tumours subcutaneously implanted as xenografts in nu/nu mice inhibited tumour growth, and in some cases caused complete regression. It is concluded that tumour growth suppression induced by rSFV was due to apoptosis induction and that the vector has an inherent cell death-promoting and antitumour activity. These results, as well as previous work by other authors on targeting and immune stimulation using alphavirus vectors, indicate that SFV recombinant particles in particular have considerable potential for further exploitation as a cancer therapy agent.
Insights
Semliki Forest virus (SFV) recombinant particles show promise as a cancer therapy. These SFV vectors inherently induce apoptosis, leading to tumor growth suppression and regression in preclinical models.
Area of Science:
- Oncolytic virology
- Gene therapy vectors
- Viral oncology
Background:
- Semliki Forest virus (SFV) is a transient RNA-based expression vector.
- SFV and its derived vectors can induce p53-independent apoptosis.
- Apoptosis induction is an inherent property of the SFV vector, not dependent on heterologous gene expression.
Purpose of the Study:
- To further assess the potential of the SFV vector as a cancer therapy agent.
- To evaluate the efficacy of SFV recombinant suicide particles (rSFV) in preclinical cancer models.
- To investigate the mechanism of tumor growth suppression induced by rSFV.
Main Methods:
- Utilized cell cultures (H358a cells) and tumor xenografts in nude mice.
- Administered SFV recombinant suicide particles (rSFV) expressing EGFP.
- Assessed apoptosis induction, spheroid growth inhibition, and tumor growth suppression/regression.
Main Results:
- rSFV induced apoptosis in p53-deficient human non-small cell lung carcinoma cells (H358a).
- EGFP-expressing rSFV inhibited the growth of H358a spheroids.
- Direct injection of rSFV into H358a tumors caused significant growth inhibition and complete regression in some cases.
Conclusions:
- Tumor growth suppression by rSFV is mediated by inherent apoptosis induction.
- SFV recombinant particles possess intrinsic cell death-promoting and anti-tumor activities.
- SFV vectors demonstrate considerable potential for development as cancer therapy agents.
