Abstract
Resistance to both cytotoxic and targeted therapies is a major problem facing cancer treatment. The mechanisms of resistance to unrelated drugs share many common features, including up-regulation of detoxifying pathways, activation of pro-survival mechanisms, and ineffective induction of cell death. Oncolytic viruses (OVs) are promising biotherapeutics for cancer treatment that specifically replicate in and lyse cancer cells. In addition to direct viral lysis, the anti-tumor effects of OVs are mediated via innate and adaptive immune responses, and several adaptation mechanisms such as autophagy appear to contribute to their anti-tumor properties. Autophagy is a versatile pathway that plays a key role in cancer survival during stressful conditions such as starvation or cytotoxic drug challenges. Autophagy also plays a role in mediating innate and adaptive immune responses by contributing to antigen presentation and cytokine secretion. This role of autophagy in regulation of immune responses can be utilized to design therapeutic combinations using approaches that either stimulate or block autophagy to potentiate therapeutic efficacy of OVs. Additional studies are needed to determine optimal multimodal combination approaches that will facilitate future successful clinical implementation of OV-based therapies.
Acknowledgments
This work was supported in part by NIH grant CA192185 to J.H.
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©2015 by De Gruyter
Articles in the same Issue
- Frontmatter
- Reviews
- The intersection between viral oncolysis, drug resistance, and autophagy
- What can lipidomics tell us about the pathogenesis of Alzheimer disease?
- Minireview
- The role of the Lowe syndrome protein OCRL in the endocytic pathway
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Systematic analysis of the contribution of c-myc mRNA constituents upon cap and IRES mediated translation
- Protein Structure and Function
- The double mutation L109M and R448M of HIV-1 reverse transcriptase decreases fidelity of DNA synthesis by promoting mismatch elongation
- The role of Bni5 in the regulation of septin higher-order structure formation
- Cell Biology and Signaling
- Extracellular localization of catalase is associated with the transformed state of malignant cells
- The importin α/β-specific inhibitor Ivermectin affects HIF-dependent hypoxia response pathways
- Proteolysis
- Inactivation of human kininogen-derived antimicrobial peptides by secreted aspartic proteases produced by the pathogenic yeast Candida albicans
- Corrigendum
- Corrigendum to: Potential importance of Maackia amurensis agglutinin in non-small cell lung cancer
Articles in the same Issue
- Frontmatter
- Reviews
- The intersection between viral oncolysis, drug resistance, and autophagy
- What can lipidomics tell us about the pathogenesis of Alzheimer disease?
- Minireview
- The role of the Lowe syndrome protein OCRL in the endocytic pathway
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Systematic analysis of the contribution of c-myc mRNA constituents upon cap and IRES mediated translation
- Protein Structure and Function
- The double mutation L109M and R448M of HIV-1 reverse transcriptase decreases fidelity of DNA synthesis by promoting mismatch elongation
- The role of Bni5 in the regulation of septin higher-order structure formation
- Cell Biology and Signaling
- Extracellular localization of catalase is associated with the transformed state of malignant cells
- The importin α/β-specific inhibitor Ivermectin affects HIF-dependent hypoxia response pathways
- Proteolysis
- Inactivation of human kininogen-derived antimicrobial peptides by secreted aspartic proteases produced by the pathogenic yeast Candida albicans
- Corrigendum
- Corrigendum to: Potential importance of Maackia amurensis agglutinin in non-small cell lung cancer