Work

Propranolol enhances the oncolytic effect of newcastle disease virus on canine mammary tumor cell by modulating the IFN-I-mediated JAK-STAT signaling pathway

Year: 2026

Type: article

Abstract: Canine mammary tumors (CMT), the most common neoplasms in intact female dogs, lack effective treatments for advanced cases. Newcastle disease virus (NDV), an oncolytic virus, kills tumor cells directly and stimulates antitumor immunity. However, NDV also activates Type I interferon (IFN-I) signaling, which restricts its replication via the JAK-STAT pathway. This study investigated whether propranolol, known to suppress antiviral responses, could enhance NDV's oncolytic effect in CMT. In vitro, using the CMT-U27 cell line, the combination reduced cell viability, migration, and invasion. Propranolol increased NDV replication and suppressed NDV-induced IFN-I release and JAK-STAT signaling pathway activation. In the CMT-U27 xenograft model, both NDV alone and the combination therapy prolonged the survival and suppressed tumor growth, with no significant difference between the two. However, the combination markedly enhanced intratumoral NDV replication by inhibiting IFN-I production and the JAK-STAT signalling pathway. These findings indicate that propranolol enhances NDV-mediated oncolysis in CMT by inhibiting the IFN-I/JAK-STAT pathway, increasing viral load, and represents a promising combined therapeutic strategy.

Source: Veterinary Quarterly

DOI: 10.1080/01652176.2026.2648283

Authors: Yunjie Zhu, Muyao Xu, Meng Li

Institution: Nanjing Agricultural University

Language: English

Topic: Virus-based gene therapy research

Subfield: Genetics

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $1,533