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Abstract <p><b>Objective:</b> The oncolytic effect of wild-type Newcastle disease virus (NDV) strains has been shown on cell lines and in animal models. Here we investigated NDV in syngeneic murine Lewis lung carcinoma (LLC) model. Fourteen days after subcutaneous tumor induction, mice received NDV intratumorally and intravenously during 4 days. The goal of the present research is to demonstrate the in vitro and in vivo ability of NDV to influence the viability of tumor cells after infection and evaluate the NDV-mediated antitumor cell death mechanism against Lewis lung carcinoma. Intravenous NDV virotherapy significantly prolonged median survival of LLC-bearing mice. <b>Results:</b> Based on the results of immunohistochemical analysis we showed necroptosis cell death induction in LLC tumor after NDV virotherapy. We showed that the expression of RIP1, and phosphorylated (Ser345) MLKL protein was significantly higher in both intravenously and intratumorally NDV-treated tumors compared to control LLC-tissue. In addition there was no expression of caspase-8, confirming the activation of necroptosis. At the same observation points we also demonstrated the apoptotic activation in LLC tumor after NDV virotherapy. We found positive IHC staining of key caspase-3 of programmed apoptotic pathway. <b>Conclusion:</b> We describe the therapeutic activity of intravenous NDV against LLC tumors as more effective for oncolytic virotherapy.</p>

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Oncolytic Virotherapy with Mesogenic Newcastle Disease Virus for Lewis Lung Carcinoma

  • 期刊论文

  • 发表日期：

    2025年6月25日

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  • K. S. Yurchenko,
  • L. S. Adamenko,
  • A. V. Glushchenko,
  • A. M. Shestopalov

摘要

Abstract

Objective: The oncolytic effect of wild-type Newcastle disease virus (NDV) strains has been shown on cell lines and in animal models. Here we investigated NDV in syngeneic murine Lewis lung carcinoma (LLC) model. Fourteen days after subcutaneous tumor induction, mice received NDV intratumorally and intravenously during 4 days. The goal of the present research is to demonstrate the in vitro and in vivo ability of NDV to influence the viability of tumor cells after infection and evaluate the NDV-mediated antitumor cell death mechanism against Lewis lung carcinoma. Intravenous NDV virotherapy significantly prolonged median survival of LLC-bearing mice. Results: Based on the results of immunohistochemical analysis we showed necroptosis cell death induction in LLC tumor after NDV virotherapy. We showed that the expression of RIP1, and phosphorylated (Ser345) MLKL protein was significantly higher in both intravenously and intratumorally NDV-treated tumors compared to control LLC-tissue. In addition there was no expression of caspase-8, confirming the activation of necroptosis. At the same observation points we also demonstrated the apoptotic activation in LLC tumor after NDV virotherapy. We found positive IHC staining of key caspase-3 of programmed apoptotic pathway. Conclusion: We describe the therapeutic activity of intravenous NDV against LLC tumors as more effective for oncolytic virotherapy.