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Peer-reviewed veterinary case report

Propranolol helps virus kill canine mammary tumor cells better

By Yunjie Zhu et al.·Published in Veterinary Quarterly·2026·Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, People's Republic of China, GB·View original on DOAJ

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

Species:
dog

Plain-English summary

A study looked at how a combination of propranolol, a medication that can reduce immune responses, and Newcastle disease virus (NDV), which can kill cancer cells, might help treat canine mammary tumors in dogs. The researchers found that using propranolol with NDV improved the virus's ability to replicate and attack tumor cells in lab tests. In a model that mimicked canine mammary tumors, both NDV alone and the combination treatment helped slow tumor growth and extended survival. The combination therapy showed a significant increase in the effectiveness of NDV against the tumors, suggesting it could be a promising new treatment option for dogs with this type of cancer.

People also search for: dog mammary tumor treatment · propranolol for dog cancer · Newcastle disease virus for canine tumors

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.

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Original publication on DOAJ: https://doi.org/10.1080/01652176.2026.2648283