Cancer management and research · 2026
Oncolytic Vaccinia Virus-Engineered EVs Convert Tumor-Promoting Macrophages into Anti-Tumor Effectors.
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Chen Liqiong, Ye Luyi, Bao Liuqian, Wang Junwei, Tan Mingming
Аннотация
INTRODUCTION: Extracellular vesicles (EVs) play a critical role in shaping the tumor immune microenvironment (TME) by mediating intercellular communication and transferring oncogenic proteins, microRNAs, and immunosuppressive molecules. Tumor-derived EVs (TDEVs) typically promote immune evasion by inducing M2 macrophage polarization, suppressing cytotoxic T-cell activity, and enhancing angiogenesis. Recent evidence suggests that oncolytic viruses (OVs) can reprogram EV secretion, generating OV-derived EVs (OV-EVs) with immunostimulatory properties capable of activating antitumor immune responses.
METHODS: In this study, we investigated how infection with oncolytic vaccinia virus (OVV) alters the EV secretion profile of colon cancer cells. EVs derived from OVV-infected tumor cells were isolated and characterized, and their effects on macrophage polarization were evaluated using in vitro assays.
RESULTS: Our results demonstrate that OVV infection significantly alters the composition and immunological properties of tumor-derived EVs. OV-EVs were enriched with pathogen-associated and damage-associated molecular patterns (PAMPs/DAMPs), which promoted macrophage reprogramming toward a pro-inflammatory M1 phenotype and enhanced immune activation associated with antitumor responses.
DISCUSSION: These findings indicate that OVV-induced EVs can reshape the tumor immune microenvironment by modulating macrophage polarization. This study provides new insights into the EV-mediated mechanisms of oncolytic virotherapy and highlights the potential of OV-derived EVs as a novel strategy for EV-based cancer immunotherapy.
METHODS: In this study, we investigated how infection with oncolytic vaccinia virus (OVV) alters the EV secretion profile of colon cancer cells. EVs derived from OVV-infected tumor cells were isolated and characterized, and their effects on macrophage polarization were evaluated using in vitro assays.
RESULTS: Our results demonstrate that OVV infection significantly alters the composition and immunological properties of tumor-derived EVs. OV-EVs were enriched with pathogen-associated and damage-associated molecular patterns (PAMPs/DAMPs), which promoted macrophage reprogramming toward a pro-inflammatory M1 phenotype and enhanced immune activation associated with antitumor responses.
DISCUSSION: These findings indicate that OVV-induced EVs can reshape the tumor immune microenvironment by modulating macrophage polarization. This study provides new insights into the EV-mediated mechanisms of oncolytic virotherapy and highlights the potential of OV-derived EVs as a novel strategy for EV-based cancer immunotherapy.