Targeting autophagy to enhance oncolytic virus-based cancer therapy

Songshu Meng1, Jiansheng Xu, Yantao Wu

  • 1Dalian Medical University Cancer Center, Institute of Cancer Stem Cell, 9 Lvshun Road South, Dalian 116044, Chin. ssmeng@yzu.edu.cn

Abstract

Insights

Oncolytic viruses (OVs) interact with cellular autophagy. Modulating autophagy, using inducers or inhibitors, can enhance OV antitumor effects, offering a promising strategy for novel cancer therapies.

Area of Science:

  • Oncology
  • Virology
  • Cell Biology

Background:

  • Autophagy is a fundamental cellular process for maintaining homeostasis.
  • Oncolytic viruses (OVs) disrupt cellular autophagy during infection of tumor cells.
  • Pharmacological modulation of autophagy shows potential in preclinical OV therapy.

Purpose of the Study:

  • To review the interactions between OVs and autophagy.
  • To summarize autophagy's role in OV replication and tumor cell lysis.
  • To explore autophagy modulation as an anticancer strategy.

Main Methods:

  • Literature review of OV-autophagy interactions.
  • Analysis of studies using autophagy inducers (e.g., rapamycin) and inhibitors (e.g., chloroquine).
  • Examination of OV-induced cytotoxicity and oncolysis.

Main Results:

  • Autophagy plays a dual role in OV replication and OV-mediated cell death.
  • Targeting autophagy can significantly enhance OV antitumor efficacy.
  • Understanding the molecular interplay is key for optimizing combination therapies.

Conclusions:

  • Modulating autophagy presents a viable therapeutic strategy to boost OV antitumor effects.
  • Further research into the OV-autophagy molecular mechanisms is warranted.
  • Combination of OVs with autophagy modulators holds significant therapeutic potential.

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