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The Antitumor Effect of Oncolytic Respiratory Syncytial Virus Via the Tumor Necrosis Factor-Alpha Induction and Ros-Bax-Mediated Mechanisms Publisher Pubmed



Samadi M1 ; Mokhtariazad T1 ; Nejati A1 ; Noroozbabaei Z1 ; Foroushani AR2 ; Haghshenas MR4 ; Adjaminejad F1 ; Zargaran H3 ; Salimi V1 ; Ghaemi A3
Authors
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Authors Affiliations
  1. 1. Virology Department, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Statistics and Epidemiology, School of Public Health, Tehran University of medical sciences, Tehran, Iran
  3. 3. Department of Influenza and Other Respiratory Viruses, Pasteur Institute of Iran, Tehran, Iran
  4. 4. Department of Microbiology, Molecular, and Cell-Biology Research Center, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran

Source: BMC Cancer Published:2023


Abstract

Background: Cervical cancer represents one of the most prevalent cancers among women worldwide, particularly in low- and middle-income nations. Oncolytic viruses (OVs) can infect cancer cells selectively and lethally without harming normal cells. Respiratory syncytial virus (RSV) is an oncolytic virus for anticancer therapy because of its propensity to multiply within tumor cells. This research aimed to assess the in vitro antitumor activities and molecular basis processes of the oncolytic RSV-A2 on the TC-1 cancer cells as a model for HPV‑related cervical cancers. Methods: Cellular proliferation (MTT) and lactate dehydrogenase (LDH) release assays were used to investigate the catalytic impacts of RSV-A2 by the ELISA method. Real-time PCR and flow cytometry assays were utilized to assess apoptosis, autophagy, intracellular concentrations of reactive oxygen species (ROS), and cell cycle inhibition. Results: Our MTT and LDH results demonstrated that TC-1 cell viability after oncolytic RSV-A2 treatment was MOI-dependently and altered significantly with increasing RSV-A2 virus multiplicity of infection (MOI). Other findings showed that the RSV-A2 potentially resulted in apoptosis and autophagy induction, caspase-3 activation, ROS generation, and cell cycle inhibition in the TC-1 cell line. Real-time PCR assay revealed that RSV-A2 infection significantly elevated the Bax and decreased the Bcl2 expression. Conclusions: The results indicated that oncolytic RSV-A2 has cytotoxic and inhibiting effects on HPV-associated cervical cancer cells. Our findings revealed that RSV-A2 is a promising treatment candidate for cervical cancer. © 2023, BioMed Central Ltd., part of Springer Nature.
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